The DOI matches its Crossref record; 63 of the 64 references it cites were found in a registry or an index, and 1 are not checked yet; 15 of the 51 sources its claims cite were checked for support.
MicroRNA 21 Promotes Glioma Invasion by Targeting Matrix Metalloproteinase Regulators
Open accessAbstract
Substantial data indicate that microRNA 21 (miR-21) is significantly elevated in glioblastoma (GBM) and in many other tumors of various origins. This microRNA has been implicated in various aspects of carcinogenesis, including cellular proliferation, apoptosis, and migration. We demonstrate that miR-21 regulates multiple genes associated with glioma cell apoptosis, migration, and invasiveness, including the RECK and TIMP3 genes, which are suppressors of malignancy and inhibitors of matrix metalloproteinases (MMPs). Specific inhibition of miR-21 with antisense oligonucleotides leads to elevated levels of RECK and TIMP3 and therefore reduces MMP activities in vitro and in a human model of gliomas in nude mice. Moreover, downregulation of miR-21 in glioma cells leads to decreases of their migratory and invasion abilities. Our data suggest that miR-21 contributes to glioma malignancy by downregulation of MMP inhibitors, which leads to activation of MMPs, thus promoting invasiveness of cancer cells. Our results also indicate that inhibition of a single oncomir, like miR-21, with specific antisense molecules can provide a novel therapeutic approach for "physiological" modulation of multiple proteins whose expression is deregulated in cancer.
Verified 2026-10-19 · 1 reference not checked yet
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
miR-21 is elevated in high-grade gliomas and promotes glioma invasion by directly targeting the MMP inhibitor RECK and indirectly regulating TIMP3, leading to increased MMP activity. Inhibiting miR-21 raises RECK/TIMP3, reduces MMP activity in vitro and in vivo, and decreases glioma cell motility and invasion, partly rescued by RECK knockdown.
Key findings
- miR-21 levels remain low in grade II gliomas and most grade III tumors but are significantly higher in GBMs; RECK mRNA is significantly lower in GBMs than normal brain and grade II/III gliomas, and TIMP3 mRNA tends to be lower in GBMs.
- Anti-miR-21 treatment changed expression of ∼570 genes (P < 0.05); upregulated transcripts were enriched for miR-21 seed hexamers (expectations 1.45e−09, 1.37e−14, and 1.82e−12), and at least 65 mRNAs were upregulated by anti-miR-21 and downregulated by miR-21 overexpression.
- miR-21 inhibition increased RECK mRNA ∼2-fold and TIMP3 mRNA about 1.6-fold; RECK was validated as a direct miR-21 target by luciferase reporter, whereas TIMP3 was not consistently directly responsive and is likely downstream.
- miR-21 inhibition reduced MMP-2 activity in A172 and U87 cells and lowered MMP activity in U87 subcutaneous tumors in nude mice; it also reduced scratch motility and Matrigel invasion, with reduced motility partly rescued by RECK siRNA and reduced invasion not observed when anti-miR-21 was cotransfected with RECK siRNA.
Methods
- Human glioma cell lines A172, U87, and LN229 (high miR-21), plus HeLa, MCF7, and U2OS cells, and human nonneoplastic brain and tumor samples; cells were transfected with 2′-O-MOE anti-miR-21, mismatch/control oligonucleotides, synthetic miR-21 duplex, or RECK siRNA.
- mRNA profiling used Agilent 44K arrays at 6 and 24 h posttreatment, with qRT-PCR, Western blot, luciferase 3′ UTR reporter assays with mutated miR-21 binding sites, gelatin zymography, scratch migration, and Matrigel invasion assays.
- In vivo, U87 cells transfected with anti-miR-21 or control were implanted subcutaneously in nude mice; MMP activity was imaged with MMPSense 680 at 3 days after implantation and 24 h later, with caliper tumor measurements.
Limitations
- Stated by the authors: the 2′-O-MOE anti-miR-21 did not significantly or consistently change glioma cell viability or reduce subcutaneous U87 tumor growth; subcutaneous U87 tumors are noninfiltrative, noninvasive, and poorly vascularized, so they are not an accurate model for studying invasiveness and tumor growth; nucleic acid chemistry can profoundly alter cellular responses to miRNA inhibition; therapeutic potential requires future research.
- Stated/evident from the text: the TIMP3 3′ UTR reporter did not consistently respond to miR-21 changes, so TIMP3 is likely a downstream effector rather than a direct target; RECK protein bands were not detectable by Western blot in U87 cells despite ∼2-fold RECK mRNA upregulation.
- Evident from the text: in vivo imaging was performed within the first week, when anti-miR-21 did not affect subcutaneous U87 tumor growth; comparison with a prior intracranial LNA-DNA anti-miR-21 study is limited because tumor locations differed.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
35 Own result · 20 Own interpretation · 18 No full text of the sources · 6 Supported · 6 Own method · 4 Supported so far · 4 Partly supported · 2 No basis given · accuracy not yet measured
Every source the paper cites for this claim was checked and supports it.
In the paper
“Among the molecules tested, the 2′-O-MOE ASO was the most potent in repressing miR-21 activity (Fig. 2A), in agreement with previous data (10), whereas the uniform 2′-O-methyl ASO was the least potent, and mixed locked nucleic acid (LNA)-DNA oligonucleotides were variable (data not shown).”
What the sources say
- Supportedcites [10] source
The Discussion explicitly identifies the uniformly modified 2′-O-MOE-PO oligonucleotide as the best anti-miRNA ASO tested. This supports the attributed comparison for miR-21 activity, although the passage specifies the oligonucleotide’s backbone as PO. (LLM, conf=0.94)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Concurring with previously published reports (12, 46), our data indicate that these MMP inhibitors regulate MMP activity posttranslationally.”
What the sources say
- Supportedcites [12] source
The paper describes TIMPs as inhibitors of metalloproteinase activity and shows that TIMP-3 controls the cell-surface activation of pro-MMP-2 (Abstract and Discussion; page numbers unavailable). Its gene-expression analysis found comparable MMP-2 levels in wild-type and TIMP-3-deficient cells despite altered processing, supporting regulation after translation. (LLM, conf=0.91)
- Not checked — no full text of the sourcecites [46] source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: MMPs are a group of peptidases involved in degradation of the ECM.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“However, we have not detected any correlation between miR-21-modulated expression in several glioma cell lines and protein level of phosphatase and tensin homolog (data not shown), the reported miR-21 target in hepatocellular carcinomas (44).”
What the sources say
- Supportedcites [44] source
The citation supports the identification of PTEN as a reported miR-21 target in hepatocellular carcinoma: the Results state that PTEN was shown to be a direct target of miR-21 in HCC cells. The preceding statement about no correlation in glioma cell lines is the citing authors’ own unpublished observation, not a finding attributed to this source. (LLM, conf=0.94)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Our data suggest that this can be at least partly due to miR-21 regulation, in addition to the reported chromosome 12q22-23 loss of heterozygosity and hypermethylation (56).”
What the sources say
- Partly supportedcites [56] Watanabe T., 2003, Brain Pathol. sourceExperimental — accuracy not yet measured
The Abstract (page unavailable) reports chromosome 12q22–23 loss of heterozygosity in glioblastomas and its association with low Apaf-1 expression. It mentions hypermethylation only as a possible mechanism in some malignancies; the reported study did not measure it in glioblastomas. The miR-21 proposal is presented as the citing authors’ own conclusion, not as a finding attributed to this source. (LLM, conf=0.83)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In gliomas, APAF1 is often inactivated or downregulated (56).”
What the sources say
- Partly supportedcites [56] Watanabe T., 2003, Brain Pathol. sourceExperimental — accuracy not yet measured
The Abstract reports low APAF1 mRNA and protein expression in many glioblastomas with chromosome 12q22–23 loss of heterozygosity. The study examined glioblastoma, however, so it does not establish that APAF1 is often inactivated or downregulated across gliomas generally. (LLM, conf=0.85)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The numbers of invasive A172 and U87 cells in cultures with inhibited miR-21 were significantly reduced relative to those in cultures transfected with the control oligonucleotide (Fig. 7A and B).”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Specific inhibition of miR-21 with antisense oligonucleotides leads to elevated levels of RECK and TIMP3 and therefore reduces MMP activities in vitro and in a human model of gliomas in nude mice.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Moreover, downregulation of miR-21 in glioma cells leads to decreases of their migratory and invasion abilities.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“RECK mRNA expression was significantly lower in GBMs than in normal brain tissue and, especially, in grade II and III gliomas.”
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“When miR-21 was suppressed, the amount of gelatin digested that reflects the levels of MMP-2 proteolytic activity was significantly reduced relative to the amount for the cells transfected with the control oligonucleotide (Fig. 5A).”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 28
- Probably not a substantial claim. 21
- The quote only partly states this claim. 2
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Accumulated data suggested that MMP levels and activities are significantly elevated in human gliomas, which contributes to glioma cell invasion of the surrounding normal tissues, metastasis, and angiogenesis through cell surface ECM degradation (21, 45).”
What the sources say
- Not checked — no full text of the sourcecites [21] Hu B., 2003, Proc. Natl. Acad. Sci. USA source
- Partly supportedcites [45] sourceExperimental — accuracy not yet measured
The Abstract and §4.1 link elevated MMP levels in human gliomas to invasiveness, and describe ECM degradation and cell-surface activation. But the Abstract discusses metastasis in cancer generally, not specifically gliomas; §4.2 links MMP-9 to angiogenesis only tentatively and says its activity in invasive glioma tissue is unproven. The copy therefore does not establish significantly elevated MMP activities across human gliomas or the claimed glioma metastasis and angiogenesis mechanism. Page numbers were not supplied. (LLM, conf=0.88)
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: MMPs are a group of peptidases involved in degradation of the ECM.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“TIMP3 is a tissue inhibitor of MMPs that inhibits angiogenesis and tumor cell infiltration and also induces apoptosis (2, 48).”
What the sources say
- Partly supportedcites [2] sourceExperimental — accuracy not yet measured
The paper’s Summary (p. 1347) identifies TIMP-3 as a tissue inhibitor of metalloproteinases, and its discussion reports inhibited invasion of HeLa and HT1080 cancer cells and apoptotic death in three cancer cell lines. The copy does not report that TIMP-3 inhibits angiogenesis; searches for angiogenesis and blood-vessel formation found no supporting passage. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [48] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“This microRNA has been implicated in various aspects of carcinogenesis, including cellular proliferation, apoptosis, and migration.”
- Also stated in: § Abstract · plain
“miR-21 has been identified in controlling apoptosis, cell proliferation, and migration of cell lines in breast, colorectal, and other cancers (1, 44, 51, 59).”
What the sources say
- Not checked — no full text of the sourcecites [1] source
- Supportedcites [44] source
The Results report that changing miR-21 expression affects proliferation and migration in HCC cells. The Discussion also reports anti-apoptotic properties of miR-21 in glioblastoma and cholangiocarcinoma, supporting the broader statement that it has been implicated in all three processes. (LLM, conf=0.92)
- Not checked — no full text of the sourcecites [51] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Also stated in: § Abstract · plain
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Our analysis also confirmed tropomyosin 1 (TPM1) regulation by miR-21, previously reported to occur in MCF7 cells (59, 60).”
What the sources say
- Supportedcites [59] source
The Abstract reports that experiments using tumors derived from MCF-7 cells identified TPM1 as a miR-21 target and confirmed that miR-21 down-regulates its expression. The Results section also reports increased endogenous TPM1 in anti-miR-21-treated, MCF-7-derived tumors. The paper therefore supports the cited prior report, although its tumor measurements were made in MCF-7-derived tumors rather than isolated cells. (LLM, conf=0.90)
- Not checked — no full text of the sourcecites [60] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Another factor that can induce miR-21 expression is hypoxia, a general feature of all solid tumors (30).”
What the sources say
- Supportedcites [30] source
The Results report miR-21 among the hypoxia-regulated microRNAs and say its microarray result was checked by quantitative RT-PCR. The introductory passage describes hypoxia as an essential feature of the neoplastic microenvironment. (LLM, conf=0.90)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The miR-21 gene contains two conserved STAT3 binding sites within its enhancer region and is induced by interleukin 6 (IL-6) in a STAT3-dependent way.”
What the sources say
- Supportedcites [39] source
The Results and discussion section identifies two conserved Stat3 binding sites in the miR-21 upstream regulatory region. It also reports that IL-6 increased miR-21 expression and that Stat3 knockdown inhibited this induction. (LLM, conf=0.94)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“MMPs can degrade ECM components and therefore play important roles in mediating GBM tumor cell motility and invasion (45).”
What the sources say
- Supportedcites [45] source
The Introduction says MMPs can degrade nearly all ECM macromolecules in the brain and are believed to play a major role in tumor invasion. The Abstract links MMP-mediated ECM degradation to glioblastoma invasion, while Section 4 describes how ECM degradation may permit glioma-cell migration. (LLM, conf=0.92)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“APAF1 (apoptotic protease activating factor 1) is the molecular core of apoptosome. It is typically required for activation of the caspases that initiate apoptosis (3, 26).”
What the sources say
- Supportedcites [3] source
The Introduction describes Apaf-1 oligomerization as forming the apoptosome, while the Results and discussion state that Apaf-1 normally recruits and activates caspases-9 and -3. The Concluding remarks add that caspase-9 activity depends on interaction with oligomerized Apaf-1. Page numbers are not provided in our copy. (LLM, conf=0.90)
- Supportedcites [26] Johnson C. E., 2007, Proc. Natl. Acad. Sci. USA source
The paper’s introductory discussion (page not specified in our copy) says cytochrome c binds Apaf-1, leading to recruitment of procaspase-9 and formation of the apoptosome; the apoptosome then activates caspase-9. In the section on Apaf-1 expression levels (page not specified), adding Apaf-1 enabled cytochrome c to activate caspases in neural extracts, supporting its required role in the pathway described. (LLM, conf=0.91)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Elevated miR-21 expression has been causally linked to proliferation, apoptosis, and migration of several cancer cell lines (1, 5, 44, 60).”
What the sources say
- Not checked — no full text of the sourcecites [1] source
- Not checked — no full text of the sourcecites [5] source
- Supportedcites [44] source
The Results report that experimentally increasing or inhibiting miR-21 changed proliferation and migration in HCC cell lines. The Discussion reports anti-apoptotic properties of miR-21 in glioblastoma and cholangiocarcinoma, supporting the apoptosis part as a finding the paper reports from other studies. (LLM, conf=0.87)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“miR-21 levels remain low in grade II gliomas and in most grade III tumors and are significantly higher in GBMs (Fig. 1).”
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“This expression pattern is different from those of the other cancer-associated miRNAs, for example, miR-10b, which is often elevated in grade III and even grade II gliomas (Fig. 1) and dysregulated in some other cancers (41).”
What the sources say
- Not checked — no full text of the sourcecites [41] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“RECK mRNA level increased consistently ∼2-fold and TIMP3 mRNA about 1.6-fold in the cells transfected with anti-miR-21.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These experiments demonstrated that inhibition of miR-21 reduced the motility of glioma cells (Fig. 6B and C).”
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The quote only partly states this claim.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“We note that, though 2′-O-MOE miR-21 ASO induced many proapoptotic and cell cycle arrest genes (Fig. 2C; also see Table S1 in the supplemental material), it did not significantly and consistently change the viability of glioma cell lines, which was reported for other, less potent miR-21 inhibitors (5, 8).”
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“STAT3, the other gene that may play a tumor suppressor function in GBM (11), is also negatively regulated by miR-21 according to the microarray data (see Table S1 in the supplemental material) and is a predicted miR-21 target (29, 34).”
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“As identified in our study, TIMP3 or both TIMP3 and RECK are also induced by anti-miR-21 in MCF7 (breast carcinoma) and U2OS (osteosarcoma) cells (Fig. 4D).”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In glioma progression from less invasive grade II gliomas to very invasive GBMs, RECK and TIMP3 levels drop (Fig. 4B), whereas miR-21 expression increases (Fig. 1).”
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Here, we show that a 2′-O-MOE ASO not only is potent but also upregulates miR-21 seed-containing mRNAs (Fig. 2 and 3).”
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Substantial data indicate that microRNA 21 (miR-21) is significantly elevated in glioblastoma (GBM) and in many other tumors of various origins.”
- Also stated in: § Abstract · boosted
“Using high-throughput profiling of miRNA expression, we have previously identified a specific miRNA, miRNA 21 (miR-21), as most strongly elevated in nearly all analyzed human GBM specimens (5).”
- Also stated in: § Abstract · boosted
“Other groups demonstrated overexpression of this miRNA in a wide range of other cancers, including breast, lung, colon, prostate, pancreas, ovarian, and stomach cancers, as well as in chronic lymphocytic leukemia (33, 54).”
What the sources say
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Also stated in: § Abstract · boosted
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“mRNAs carrying RECK and TIMP3 are predicted conserved miR-21 targets with one and two putative binding sites, respectively (Fig. 4A).”
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The sequences of the control and mismatch oligonucleotides have been analyzed using BLAST searches to exclude potential hits in the human transcriptome.”
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“RECK is a membrane-anchored MMP inhibitor whose reduced expression or inactivation seems to be critical for the invasiveness and metastasis of various cancers, including glioma cancer (7, 46).”
What the sources say
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The high level of miR-21 expression in GBMs compared to that in anaplastic astrocytomas suggests the involvement of miR-21 in one of these key processes.”
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The quote only partly states this claim.
In the paper
“Its expression level is also an important prognostic factor for multiple cancer types (6).”
What the sources say
- Not checked — no full text of the sourcecites [6] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“It has been demonstrated to inhibit MMP activity and tumor growth in malignant gliomas in vivo (31, 32).”
What the sources say
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Since modified oligonucleotides can induce a wide range of nonspecific, off-target-mediated effects, several ASO molecules of different chemistries have been used for miR-21 inhibition.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Our data suggest that miR-21 contributes to glioma malignancy by downregulation of MMP inhibitors, which leads to activation of MMPs, thus promoting invasiveness of cancer cells.”
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: MMPs are a group of peptidases involved in degradation of the ECM.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Such overrepresentation of the hexamers suggests an abundance of direct miR-21 targets among the genes upregulated by 2′-O-MOE anti-miR-21 and indicates that the effects of this molecule on glioma cells are indeed mediated through the miR-21 pathway.”
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“These experiments have been performed with the miR-21 inhibitor and with a mismatched control oligonucleotide to ensure that any observed effects are driven by miR-21.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
In the paper
“Importantly, it inhibits tumor necrosis factor alpha-converting enzyme and induces apoptosis through the stabilization of tumor necrosis factor alpha receptors on the cell surface (42).”
What the sources say
- Not checked — no full text of the sourcecites [42] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Moreover, it leads to reduction of glioma cell motility and invasion, which is mediated by elevated RECK expression and was partly rescued by RECK siRNA (Fig. 6 and 7).”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This implies that miR-21 regulates RECK and TIMP3 expression and thus MMP activities and glioma tumor invasiveness.”
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In this study, we have demonstrated in vitro and in vivo, using U87 glioma xenografts in nude mice, that miR-21 regulates MMPs and glioma cell invasiveness by directly controlling the MMP inhibitor RECK.”
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These combined results indicate that miR-21 regulates overlapping though not identical sets of genes in different cells and therefore shares common signaling pathways in different cancers.”
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The APAF1 3′ UTR contains a strong miR-21 binding site (9-mer binding at miR-21 5′ end), and therefore, it is likely one of the direct miR-21 targets.”
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Its expression is highly upregulated in a variety of solid tumors, including GBM, breast, lung, colon, prostate, pancreas, and stomach cancers (5, 54).”
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Our mRNA expression analysis suggests that miR-21 regulates the expression of multiple mRNA targets and thereby induces several cellular programs in glioma cells, including those associated with the tumor invasiveness and microvascular proliferation typical for the GBM as well as those involved in cell cycle regulation and apoptosis.”
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Its ectopic expression in glioma cells induces upregulation of genes associated with angiogenesis, growth factors, cytokines, death receptors, and substrates of the various MMPs (31).”
What the sources say
- Not checked — no full text of the sourcecites [31] Lam P., 2005, Mol. Ther. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“RECK, a membrane-anchored regulator, and TIMP3, the ECM-bound protease regulator, are key inhibitors of several MMPs, and their expression is prognostic in a number of common cancers (28, 53).”
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“TIMP3 has been demonstrated to activate caspases and therefore induce apoptosis of human glioma cells in vitro and the growth inhibition of human glioma tumors in a mouse model (31, 32).”
What the sources say
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Though mRNA expression analysis does not allow identification of targets whose translation is regulated without modulation of mRNA levels”
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Such a bidirectional approach to manipulating miR-21 levels enabled narrowing of the lists of regulated genes and identification of those whose expression correlated negatively with miR-21 levels”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In these experiments, we used tumorigenic U87 cells, a common model of human gliomas (23).”
What the sources say
- Not checked — no full text of the sourcecites [23] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper relies on this without support.
MMPs are a group of peptidases involved in degradation of the ECM.
“MMPs are a group of peptidases involved in degradation of the ECM.”
The paper relies on this without support.
Subcutaneous U87 tumors are noninfiltrative, noninvasive, and poorly vascularized.
“We should also note that subcutaneous U87 tumors are noninfiltrative, noninvasive, and poorly vascularized.”
The paper relies on this without support.
Knowledge of the molecular mechanisms mediating miR-21 function in cancer generally and in gliomas specifically is limited.
“However, our knowledge of the molecular mechanisms mediating miR-21 function in cancer generally and gliomas specifically is limited.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“miR-21 is a well-known miRNA, found to be overexpressed in almost all cancer types, where its upregulation promotes cell proliferation, invasion, and metastatic behavior.”
From Potential Therapeutic Effects of Exosomes Packed With a miR-21-Sponge Construct in a Rat Model of Glioblastoma (2019) · cites this paper as [17]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Previous studies have proven that PDCD4, HNRNPK and RECK are TSGs among the direct targets of miR-21-5p (13,(27)(28)(29).”
From Functional interaction between miR-505-3p and miR-21 contributes to GBM suppression (2026) · cites this paper as [28]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“miR-21 targets several genes such as PDCD4, TIMP3, and RECK, which are key regulators of apoptotic and metastatic pathways (17–23).”
From Potential Therapeutic Effects of Exosomes Packed With a miR-21-Sponge Construct in a Rat Model of Glioblastoma (2019) · cites this paper as [17]
The cited source says what the claim attributes to it.
In the citing paper
“Our data on the effects of miR-21 enriched exosomes is in agreement with the previous reports demonstrating that overexpressed miR-21 in cell lines can increase the proliferation rate and malignant behavior of the cells (17–23).”
From Potential Therapeutic Effects of Exosomes Packed With a miR-21-Sponge Construct in a Rat Model of Glioblastoma (2019) · cites this paper as [17]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ DISCUSSION
“Its overexpression by viral transduction induces apoptosis in glioma cells and may be beneficial in glioma treatment (50).”
§ REFERENCES
“50.Shinoura, N., N. Yamamoto, Y. Yoshida, A. Asai, T. Kirino, and H. Hamada. 2000. Adenovirus-mediated transfer of caspase-8 in combination with superrepressor of NF-kappaB drastically induced apoptosis in gliomas.”
Citations
Cites
Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2−ΔΔCT Method
Livak, K. J., & Schmittgen, T. D. (2001) · Methods · doi:10.1006/meth.2001.1262 · Cited by 180,860
Lewis, B. P., Burge, C. B., & Bartel, D. P. (2005) · Cell · doi:10.1016/j.cell.2004.12.035 · Cited by 11,855
Oncomirs—MicroRNAs with a role in cancer
Esquela-Kerscher, A., & Slack, F. J. (2006) · Nature Reviews Cancer · doi:10.1038/nrc1840 · Cited by 5,884
A microRNA expression signature of human solid tumors defines cancer gene targets
Volinia, S., Calin, G. A., Liu, C.-G., Ambs, S., Cimmino, A., Petrocca, F., Visone, R., Iorio, M., Roldo, C., Ferracin, M., et al. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0510565103 · Cited by 5,697
Summaries of Affymetrix GeneChip probe level data
Irizarry, R. A. (2003) · Nucleic Acids Research · doi:10.1093/nar/gng015 · Cited by 4,837
Microarray analysis shows that some microRNAs downregulate large numbers of target mRNAs
Lim, L. P., Lau, N. C., Garrett-Engele, P., Grimson, A., Schelter, J. M., Castle, J., Bartel, D. P., Linsley, P. S., & Johnson, J. M. (2005) · Nature · doi:10.1038/nature03315 · Cited by 4,755
Self-citationIn vitro scratch assay: a convenient and inexpensive method for analysis of cell migration in vitro
Liang, C.-C., Park, A. Y., & Guan, J.-L. (2007) · Nature Protocols · doi:10.1038/nprot.2007.30 · Cited by 4,696
Combinatorial microRNA target predictions
Krek, A., Grün, D., Poy, M. N., Wolf, R., Rosenberg, L., Epstein, E. J., MacMenamin, P., da Piedade, I., Gunsalus, K. C., Stoffel, M., et al. (2005) · Nature Genetics · doi:10.1038/ng1536 · Cited by 4,603
miRBase: microRNA sequences, targets and gene nomenclature
Griffiths-Jones, S. (2006) · Nucleic Acids Research · doi:10.1093/nar/gkj112 · Cited by 3,950
John, B., Enright, A. J., Aravin, A., Tuschl, T., Sander, C., & Marks, D. S. (2004) · PLoS Biology · doi:10.1371/journal.pbio.0020363 · Cited by 3,796
Research works printed but not linked: 1
- Gao F., 2007, Oncol. Rep., 17, 123
Cited by
Sorted by citations
Items 701–800 of 886
Wei, X., Zhang, Q., Liu, C., Wu, S., Nong, W., Ge, Y., Lin, L., Li, F., Xie, X., & Luo, B. (2022) · Current Medical Science · doi:10.1007/s11596-022-2593-5 · Cited by 6
Outside the limit: questioning the distance restrictions for cooperative miRNA binding sites
Diener, C., Hart, M., Fecher‐Trost, C., et al. (2023) · Cellular & Molecular Biology Letters · doi:10.1186/s11658-023-00421-4 · Cited by 6
“Likewise, previously reported effects were consistent with our data, including the formerly described regulation of RECK by miR-21-5p [30] and the regulations of LHFPL and DDX17 by miR-155-5p [15, 31].”
ResultMicro RNAs as a Diagnostic Marker between Glioma and Primary CNS Lymphoma: A Systematic Review
Ohadi, M. A. D., Aleyasin, M. S., Samiee, R., Bordbar, S., Maroufi, S. F., Bayan, N., Hanaei, S., & Smith, T. R. (2023) · Cancers · doi:10.3390/cancers15143628 · Cited by 6
“The increase in miR-21 expression may cause the inhibitors of matrix metalloproteinase (MMPs), such as RECK [38,44] and TIMP3 [34] to decrease, leading to elevated MMPs and an increased invasiveness of glioma tumor cells [45].”
BackgroundIvermectin as a potential therapeutic strategy for glioma
Hu, X., Ju, Y., & Zhang, Y. (2023) · Journal of Neuroscience Research · doi:10.1002/jnr.25254 · Cited by 7
“…in glioma patients. miR-21 is commonly overexpressed in tumors and is acknowledged as a marker of unfavorable prognosis (Asangani et al., 2008; Folini et al., 2010; Gabriely et al., 2008; Moriyama et al., 2009; Papagiannakopoulos et al., 2008; Yan et al., 2008; Yang et al., 2015; Yao & Lin, 2012).”
BackgroundSpence, T., Nguyen, J., Bouffet, É., & Huang, A. (2010) · Springer eBooks · doi:10.1007/978-94-007-0298-1_15 · Cited by 6
“Specifically, RECK and TIMP3, which are inhibitors of matrix metalloproteases (MMPs), have been shown to be directly targeted by miR-21 to promote GBM cell migration and invasion (Connolly et al. 2010; Gabriely et al. 2008).”
BackgroundInhibition of miR-21 Promotes Cellular Senescence in NT2-Derived Astrocytes
Balint, V., Ninković, D. S., Anastasov, N., Lazić, S., Kovačević‐Grujičić, N., Stevanović, M. J., & Lazic, A. (2021) · Biochemistry (Moscow) · doi:10.1134/s0006297921110079 · Cited by 8
Genetic and epigenetic markers of gliomas
Semenova, E., & Filatov, M. V. (2013) · Cell and Tissue Biology · doi:10.1134/s1990519x13040123 · Cited by 6
“Moreover, miR 21 probably regulates genes engaged in cell migration (Gabriely et al., 2008).”
BackgroundThe Involvement of Epigenetic Mechanisms in HPV‐Induced Cervical Cancer
Plesa, A., Iancu, I. V., Botezatu, A., Huică, I., Stoian, M., & Anton, G. (2016) · InTech eBooks · doi:10.5772/62833 · Cited by 6
RNA biomarkers in hemorrhagic stroke
Khavandegar, A., Ramezani, Z., Ahmadi, N. S., Azizi, N., Sharif-Alhoseini, M., & Lucke-Wold, B. P. (2025) · Advances in clinical chemistry · doi:10.1016/bs.acc.2025.11.004 · Cited by 6
The Role of Non-coding RNAs in the Pathogenesis of Glial Tumors
Kovalenko, T. F., Larionova, T. D., Антипова, Н. В., Shakhparonov, M. I., & Pavlyukov, M. S. (2021) · Acta Naturae · doi:10.32607/actanaturae.11270 · Cited by 5
Mitra, T., Prusty, M., & Elangovan, S. (2024) · Computational Biology and Chemistry · doi:10.1016/j.compbiolchem.2024.108280 · Cited by 5
Nickel Toxicity and Carcinogenesis
Brocato, J., & Costa, M. (2017) · Royal Society of Chemistry eBooks · doi:10.1039/9781788010580-00027 · Cited by 5
Rong, Y., Zhou, M., Cui, X., et al. (2017) · Journal of Occupational and Environmental Medicine · doi:10.1097/jom.0000000000001268 · Cited by 5
“Furthermore, reversion-inducing cysteinerich protein with kazal motifs (RECK), a target gene of miR-21, is an inhibitor of MMPs that regulates disease.(34) MiR-200c, a member of the miR-200 family, has been found to be decreased in a mouse model of lung fibrosis.”
BackgroundGastric Cancer MicroRNAs Meta-signature.
Zare, A., Ganji, M., Omrani, M. D., et al. (2019) · PubMed · doi:10.22088/ijmcm.bums.8.2.94 · Cited by 5
“Notably, most of these targets are tumor suppressor genes, including phosphatase and tensin homolog (PTEN), tropomyosin 1 (TPM1) and reversioninducing cysteine-rich protein with Kazal motifs (RECK) (29-31).”
BackgroundLiu, M. H., Yang, L., Xj, L., et al. (2016) · PubMed · doi:10.3760/cma.j.issn.0253-2727.2016.11.011 · Cited by 5
“[6] Gabriely G, Wurdinger T, Kesari S, et al.”
BackgroundInvolvement of miRNA-337 in Various Cancers
Fakeri, M., Koulaeizadeh, S., Armandzadeh, S. M., Beilankouhi, E. A. V., Valilo, M., & Alivand, M. R. (2023) · Current Cancer Therapy Reviews · doi:10.2174/1573394719666230518112114 · Cited by 5
Jacomasso, T., Ribas, H. T., Trombetta-Lima, M., et al. (2019) · Melanoma Research · doi:10.1097/cmr.0000000000000650 · Cited by 5
Natural Proteinaceous Inhibitors of Serine Proteases
Dębowski, D. (2012) · Current Pharmaceutical Design · doi:10.2174/1381612811319060009 · Cited by 5
“[55] on human glioma cell lines, have shown that the suppression of tumor growth is mediated by inhibition of MMPs activities.”
BackgroundYang, T., Chen, M., Wang, Y., et al. (2017) · OncoTargets and Therapy · doi:10.2147/ott.s144014 · Cited by 5
“In spite of advances in surgery, radiation therapy, and chemotherapy, the prognosis of patients with gliomas has not significantly improved, and the median survival time of patients is expected to be 12–15 months.(4,5) The unrestricted growth of glioma is not only the result of abnormal cell differentiation and prolif…”
BackgroundRetractedSun, S., Lee, D., & Leung, G. (2013) · Humana Press eBooks · doi:10.1007/978-1-62703-456-2_14 · Cited by 5
“miR-21 has been extensively studied as it is consistently up-regulated in GBM cells and plays extensive roles in apoptosis, glioma invasion, proliferation, and drug resistance [ 171 , 172 ].”
BackgroundLu, V. M., Chandar, J. S., Castro, J. R., Seetharam, D., Govindarajan, V., Ramsoomair, C. K., Desgraves, J. F., Hudson, A. J., & Shah, A. H. (2025) · British Journal of Cancer · doi:10.1038/s41416-025-03094-2 · Cited by 4
“These fi ndings collectively suggest that targeting TLR-4 can impact and attenuate GBM LMD progression from multiple perspectives.”
Kim, Y., Kang, H., & Lawler, S. E. (2014) · Springer proceedings in mathematics & statistics · doi:10.1007/978-1-4939-1793-8_6 · Cited by 4
“Glioma invasion is promoted by miR-21 through downregulation of matrix metalloprotease (MMP) inhibitors [21].”
Bušek, P., Převorovský, M., Krepela, E., & Šedo, A. (2014) · Springer eBooks · doi:10.1007/978-3-7091-1431-5_12 · Cited by 4
microRNA in the control of stem-like phenotype of cancer cells
Woźniak, M. (2013) · Open Life Sciences · doi:10.2478/s11535-013-0222-9 · Cited by 4
MicroRNA 21 Expression Levels in HIV Negative and HIV Positive Diffuse Large B Cell Lymphoma
E, P. P. M. (2015) · Hereditary Genetics · doi:10.4172/2161-1041.1000143 · Cited by 4
“miR-21 is involved in tumourigenesis [17], tumour progression [19], and metastasis [20].”
BackgroundThe Role of microRNAs in Cancer
Leva, G. D., & Croce, C. M. (2015) · Wiley eBooks · doi:10.1002/9781118468678.ch8 · Cited by 6
Regulation of angiogenesis and cancer cell proliferation by human vault RNA1-2
Gallo, S., Suspitsyna, A., Sánchez‐Taltavull, D., Fort, R. S., Duhagon, M. A., Stroka, D., & Polacek, N. (2025) · NAR Cancer · doi:10.1093/narcan/zcaf028 · Cited by 3
“For instance, miR-21 promotes tumor invasion and metastasis by targeting tumor suppressor genes, while long ncRNAs like H19 and MALAT1 modulate epithelial–mesenchymal transition and cell motility [ 17–19 ].”
Pandey, S., Dwivedi, A., Singh, R., Habib, N., Kashyap, D., Saini, V., Singh, A., Sharma, A., & Jha, H. C. (2025) · Human Gene · doi:10.1016/j.humgen.2025.201507 · Cited by 5
Glioblastoma: Current Chemotherapeutic Status and Need for New Targets and Approaches
Jain, A., James, C. K., Golam, M. I., Behar, K. L., & Bhush, A. (2011) · InTech eBooks · doi:10.5772/21050 · Cited by 3
Kim, J. H., Li, L., Cai, H., Nguyen, V. H., Min, J., Shin, B. A., Choi, S., & Koh, Y. S. (2015) · Genes & Genomics · doi:10.1007/s13258-015-0357-3 · Cited by 3
“Recently, microRNAs (miRNAs) have emerged as another regulator of MMP activities (Akhtar et al. 2010; Fang et al. 2011; Gabriely et al. 2008). miRNAs are endogenous, approximately 21-nucleotide long, non-coding RNAs that bind to miRNAs, resulting in translational repression or miRNA degradation in…”
BackgroundOnganer, P. U. (2020) · Biomedical Journal of Scientific & Technical Research · doi:10.26717/bjstr.2020.25.004241 · Cited by 3
“On the other hand, a member of the miR-200 family, miR-200c, is reported to be involved in the progression of various cancers as a tumour suppressor and inhibits PI3K-Akt pathway [8].”
BackgroundKim, G. H., Heo, H. J., Kang, J. W., Kim, E., Baek, S. E., Keun-young Kim, A., Kim, I. J., Suh, S., Lee, B., Kim, Y. H., et al. (2022) · Cancer Cell International · doi:10.1186/s12935-022-02606-x · Cited by 3
Weber, A. F., Scholl, J. N., Dias, C. K., Pierdoná, V., Assmann, T. S., Anzolin, E., Kus, W. P., Worm, P. V., Battastini, A. M. O., & Figueiró, F. (2024) · The FASEB Journal · doi:10.1096/fj.202401538r · Cited by 4
“Lower expression levels of this miRNA have been shown in grade II and III gliomas when compared to GBM samples, 48–50 corroborating our findings in grade III and GBM wt samples.”
Gene/Viral Treatment Approaches for Malignant Brain Cancer
Kim, J. W., Pituch, K. C., Xiao, A., et al. (2018) · Elsevier eBooks · doi:10.1016/b978-0-12-812100-9.00015-2 · Cited by 3
Anticancer Agents from Xanthium strumarium Fruits Against C6 Glioma Cells
Kara, I. D., Çakır, A., Özaslan, M., et al. (2022) · International Journal of Pharmacology · doi:10.3923/ijp.2022.437.454 · Cited by 3
Pan, T., & Wu, X. (2012) · Archives of Medical Research · doi:10.1016/j.arcmed.2012.04.001 · Cited by 3
MicroRNAs in Endothelial Development and Differentiation
Yang, Y. Z. F. (2014) · Journal of Stem Cell Research & Therapy · doi:10.4172/2157-7633.1000191 · Cited by 3
“Many of the target genes identified for miR-21 are well-known tumor suppressors, such as Phosphatase and Tensin Homolog (PTEN) [56], Programmed Cell Death 4 (PDCD4) [57], RECK [58], RhoB [59], Bcl-2 [60], sprouty 1/2 [61], Tropomyosin [62], Maspin [63] and so on.”
Palkina, N. V., Shvetsova, Y. I., Кириченко, А. К., et al. (2015) · Russian Journal of Archive of Pathology · doi:10.17116/patol201577141- · Cited by 3
A new and accurate continuum description of moving fronts
Johnston, S. T., Baker, R. E., & Simpson, M. J. (2017) · New Journal of Physics · doi:10.1088/1367-2630/aa5bf5 · Cited by 3
MicroRNAs in the Central Nervous System and Potential Roles of RNA Interference in Brain Tumors
Purow, B. W. (2009) · Humana Press eBooks · doi:10.1007/978-1-60327-553-8_27 · Cited by 3
Καποδίστριας, Ν., Theocharopoulou, G., & Vlamos, P. (2020) · Advances in experimental medicine and biology · doi:10.1007/978-3-030-32637-1_1 · Cited by 3
Xu, X., Liu, Y., Jiang, C. L., et al. (2025) · Cytotechnology · doi:10.1007/s10616-024-00693-4 · Cited by 2
“For instance, miR-21, miR-146b and miR-373 control the expression levels of TIMP-3, MMP-16 and MMP-9 related to cell invasion and migration, and collagen homeostasis, respectively (Gabriely et al. 2008; Liu and Wilson 2012; Xia et al. 2009).”
Mikołajczak, K., Chmiel, J., & Leszek, J. (2026) · Cells · doi:10.3390/cells15121111 · Cited by 2
“Hypoxic conditions in the glioblastoma microenvironment polarize TAMs further toward an M2 phenotype and induce them to express pro-angiogenic and immunosuppressive genes (HIF-1 can directly upregulate arginase-1 and VEGF in TAMs, for example) [123–125].”
Important miRs of Pathways in Different Tumor Types
Wuchty, S., Arjona, D., & Bauer, P. O. (2013) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1002883 · Cited by 2
“Implicated in the development of glioblastomas [49,50], knockdown of miR-21 leads to reduced cell proliferation, invasiveness, tumorigenicity and increased apoptosis [49,50,51].”
BackgroundKim, G., Park, E. C., Ryu, C. H., et al. (2011) · Journal of Analytical Science & Technology · doi:10.5355/jast.2011.97 · Cited by 2
Hu, N., Cheng, H., Zhang, K., & Jensen, R. L. (2017) · Cancer Informatics · doi:10.1177/1176935117734844 · Cited by 3
Diana, A., Gaido, G., Maxia, C., & Murtas, D. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21249630 · Cited by 2
Wei, X., You, X., Zhang, J., & Zhou, C. (2019) · Translational Cancer Research · doi:10.21037/tcr.2019.07.29 · Cited by 2
“MiR-21 downregulates the suppressor of MMPs, resulting activated MMPs to promote cell invasion and increase the malignancy of tumor (22).”
BackgroundMicroRNAs in opisthorchiids and their definitive hosts: Current Status and Perspectives
Li, X., Ding, J., Zhang, X., Zhang, X., Jiang, X., Chen, R., Cheng, Y., Sun, Y., Wan, J., Zhang, Y., et al. (2024) · Molecular and Biochemical Parasitology · doi:10.1016/j.molbiopara.2024.111636 · Cited by 2
MicroRNAs in Cancer (An Overview)
Ferracin, M., Călin, G. A., & Negrini, M. (2010) · Springer eBooks · doi:10.1007/978-94-007-0298-1_1 · Cited by 2
RNAi-based Approaches to the Treatment of Brain Tumors
Mathupala, S. P., Mittal, S., Guthikonda, M., & Sloan, A. E. (2010) · Springer eBooks · doi:10.1007/978-94-007-0298-1_22 · Cited by 2
Somasundaram, K., Rao, S. A. M., & Nawaz, Z. (2011) · InTech eBooks · doi:10.5772/23935 · Cited by 2
“In addition to its effects on growth, miR-21 also affected the property of invasion that causes infiltrating pattern of glioma growth in vivo (Gabriely et al., 2008).”
BackgroundMethodResultInfluentialThe Role of microRNAs in Gliomas and Their Potential Applications for Diagnosis and Treatment
Lavon, I. (2012) · InTech eBooks · doi:10.5772/25003 · Cited by 2
miRNA Expression and Functions in Glioma and Glioma Stem Cells
Brodie, C., Buchris, E., & Lee, H. K. (2014) · Springer eBooks · doi:10.1007/978-3-319-05134-5_2 · Cited by 2
“miR-21 is considered an oncogenic miRNA and it regulates cell migration by inhibiting RECK and TIMP3 [93] and cell apoptosis [94].”
MicroRNA epigenetic systems and cancer
Lewis, H. B., & Esquela‐Kerscher, A. (2015) · Cambridge University Press eBooks · doi:10.1017/cbo9780511979811.010 · Cited by 3
Optimizing prognosis-related key miRNA-target interactions responsible for cancer metastasis
Zhao, H., Yuan, H., Hu, J. R., Xu, C., Liao, G., Yin, W., Xu, L., Wang, L., Zhang, X., Shi, A., et al. (2017) · Oncotarget · doi:10.18632/oncotarget.22724 · Cited by 2
“It was consistent that oncogenic miR-21 and miR-155 involved in the progression and invasion of GBM [16, 34], and a set of their common key targets such as LHX6 [35], DRD1 [17], NEUROG1 [36] and RAB27B [37] were also associated with tumor progression.”
BackgroundPathogenic and Therapeutic Role of Micrornas in Glioblastoma Multiforme
Babazadeh, S. M., Zolfaghary, M. R., Shirian, S., et al. (2020) · The Neuroscience Journal of Shefaye Khatam · doi:10.29252/shefa.8.2.107 · Cited by 2
Rihane, F. E., Erguibi, D., Lamsisi, M., Chehab, F., & Ennaji, M. M. (2021) · Journal of Gastrointestinal Cancer · doi:10.1007/s12029-021-00691-1 · Cited by 2
“It has been suggested that downregulation of RECK plays a role in the progression of gastric cancer. miRNAs are now increasingly used for the early diagnosis and long-term prognosis of certain types of diseases, especially cancers.”
BackgroundInfluentialRetractedAntisense Oligonucleotides in the Treatment of Malignant Gliomas
Caruso, G., Caffo, M., Raudino, G., Raudino, F., Venza, M., & Tomasello, F. (2012) · RNA technologies · doi:10.1007/978-3-642-27426-8_9 · Cited by 3
“Moreover, miR-21 promotes glioma invasive phenotype, by regulating also genes associated not only with glioma cell apoptosis but also with migration and invasiveness, including the RECK and TIMP3 genes, inhibitors of matrix metalloproteinases (MMPs) (Gabriely et al. 2008).”
BackgroundMachine Learning-based Prediction of the Likelihood of Colorectal Cancer Using miRNA Expression
Sultan, A., de Asa, A. A., Guimbangunan, T. M., Serapio, E. D., Fellizar, A., Albano, P. M., & Tomas, R. C. (2023) · The Philippine journal of science · doi:10.56899/152.04.12 · Cited by 2
Epigenetic Profiling of Gliomas
Nagarajan, R. P., & Costello, J. (2009) · Humana Press eBooks · doi:10.1007/978-1-60327-553-8_26 · Cited by 2
MicroRNA Signatures as Biomarkers in Cancer
Adams, B. D., & Slack, F. J. (2015) · Wiley eBooks · doi:10.1002/9780470015902.a0025346 · Cited by 2
Epigenetic Mechanisms in Cancer Formation and Progression
Fratta, E., Sigalotti, L., Covre, A., Parisi, G., Danielli, R., Nicolay, H. J. M., Coral, S., & Maio, M. (2011) · Wiley eBooks · doi:10.1002/9781118005743.ch10 · Cited by 3
The role of microRNAs during hepatitis C viral infection and liver regeneration
Marquez, R. T., McCaffrey, A. P., Davidson, B. L., Stapleton, J. T., Maury, W. J., & Varga, S. M. (2009) · doi:10.17077/etd.pxz08vto · Cited by 2
Góźdź, A., Maksym, R., Ścieżyńska, A., Götte, M., Kiéda, C., Wlodarski, P. K., & Malejczyk, J. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252111594 · Cited by 1
Integrated Genomic Analysis Unveils MicroRNA Roles in Glioma Development
Majed, S. O., Abdullah, G. H., Sulaiman, K. M., Maaruf, S. M., Yashooa, R. K., Abdulla, S. S., Villa, C., & Mustafa, S. (2026) · Biology · doi:10.3390/biology15070533 · Cited by 1
“For instance, strategies aiming to inhibit oncomiR or restore tumor suppressor miRNAs could provide new avenues for targeted therapy [27,47–49].”
Status and Development Trend on Tumor Metastasis*
Qi, F., He, F., & Jiang, Y. (2009) · PROGRESS IN BIOCHEMISTRY AND BIOPHYSICS · doi:10.3724/sp.j.1206.2009.00157 · Cited by 1
Liu, J., Chi, D., Lu, H., et al. (2015) · Annals of Vascular Surgery · doi:10.1016/j.avsg.2015.01.032 · Cited by 1
Regulation of Metastasis by miRNAs
Alahari, S. K. (2012) · Springer eBooks · doi:10.1007/978-94-007-4655-8_6 · Cited by 1
Targeted Therapies in Brain Tumours: An Overview
Crilly, S. M., & O’Halloran, P. J. (2016) · Resistance to targeted anti-cancer therapeutics · doi:10.1007/978-3-319-46505-0_1 · Cited by 1
Detection of miRNA Expression Alteration in Diffuse and High Grade Glial Tumors
Süslüer, S. Y., Biray, C., Dogan, Z. O., Balcı, T., Kayabaşı, Ç., Akalın, T., Dalbastı, T., & Gündüz, C. (2015) · Journal of Neurological Sciences-turkish · Cited by 1
Astrocytomas and miRNAs: Are They Useful?
Pérezpeña-Díazconti, M., Eguía-Aguilar, P., & de León, F. C.-P. (2019) · IntechOpen eBooks · doi:10.5772/intechopen.77419 · Cited by 1
“Many other studies have confirmed the over-expression of this miR in the four grades of astrocytomas and in other tumours of the SNC as oligoastrocytoma, oligodendroglioma and medulloblastomas, having a greater expression in the multi-shaped glioblastoma (Figure 6) [26, 38, 58].”
BackgroundMicroRNAs in CANCER: MiR-21 and MiR-155
(2017) · International journal of research studies in biosciences · doi:10.20431/2349-0365.0509007
“…cell death 4 (Asangani et al., 2008; Frankel et al., 2008), maspin (Zhu et al., 2008), and matrix metalloproteinases inhibitors RECK and TIMP3 (Gabriely et al., 2008) were targets of miR-21, the whole data put together suggest that miR-21 is an important oncogenic miRNA which is closely…”
BackgroundHe, Y., Cheng, Y., Chen, M., Shi, L., Chen, T., Chen, H., & Zhang, X. (2017) · PubMed Central · Cited by 1
Sun, Z., Zhao, Y., Ding, X. Z., et al. (2020) · Translational Cancer Research · doi:10.21037/tcr-20-2487 · Cited by 1
“MiR-21 is a recognized oncogene that modulates tumor cell proliferation, migration, invasion, and apoptosis by regulating the epidermal growth factor receptor (EGFR) and matrix metalloproteinases (MMP) pathway and inhibiting programmed cell death 4 (PDCD4) expression (16-18).”
BackgroundThe Concept and Mechanisms of Metastasis
Ekmekçi, S., & Aktaş, S. (2022) · Springer eBooks · doi:10.1007/978-3-030-84432-5_2 · Cited by 1
MicroRNA Regulation of mTOR Function
Zambrotta, M. E., & Houlé, J. D. (2015) · Elsevier eBooks · doi:10.1016/b978-0-12-820719-2.00022-3 · Cited by 1
MicroRNAs in the Molecular Pathology of Gliomas
Šáňa, J., Bešše, A., & Slabý, O. (2014) · Springer eBooks · doi:10.1007/978-3-7091-1431-5_4 · Cited by 1
Leva, G. D., & Garofalo, M. (2014) · Springer eBooks · doi:10.1007/978-3-319-03725-7_5 · Cited by 1
Hypoxia Responsive Vectors Targeting Astrocytes in Glioma
Manas, R., Howard, M., & Janet, C. (2012) · InTech eBooks · doi:10.5772/24711 · Cited by 1
“Downregulation of miR-21 may be an effective strategy for blocking the expression of MMPs and for activating tissue inhibitor of metalloproteinases in glioma cells (Gabriely et al., 2008).”
BackgroundLiu, Q., Zhou, N., & Mo, Y. (2012) · Springer eBooks · doi:10.1007/978-94-007-4655-8_5 · Cited by 1
Critical Molecular and Genetic Markers in Primary Brain Tumors with Their Clinical Importance
Yaylım, İ., Azam, S., Farooqı, A. A., Küçükhüseyin, Ö., Ismail, M. S., & Kafadar, A. M. (2016) · InTech eBooks · doi:10.5772/63550 · Cited by 2
4.30 Nanomaterials for Drug Delivery to the Brain
Gaudin, A., Seo, Y.-E., Song, E., Quijano, E., King, A. R., & Saltzman, W. M. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-803581-8.09288-2 · Cited by 1
Is Use of Micro-RNA–Containing Food Feasible?
Kang, J.-W., Baek, H.-A., Cho, S., & Lee, J. (2016) · Journal of Food Chemistry and Nanotechnology · doi:10.17756/jfcn.2016-009 · Cited by 1
“For instance, miR-21 functions as an oncogene by regulating many tumor suppressor genes and is upregulated in many human malignancies [9, 10], including breast cancer [11, 12], glioblastoma [13], hepatocellular carcinoma [14], cholangiocarcinoma [15], lung cancer [16], tongue squamous cell carcinoma [17], gastric canc…”
BackgroundProspective Advances in Non-coding RNAs Investigation
Jan, M. I., Ali, T., Ishtiaq, A., Mushtaq, I., & Murtaza, I. (2020) · Advances in experimental medicine and biology · doi:10.1007/978-981-15-1671-9_24 · Cited by 1
MicroRNA Regulation of Glycolytic Metabolism in Glioblastoma
Alfardus, H., McIntyre, A., & Smith, S. J. (2020) · Vide Leaf, Hyderabad eBooks · doi:10.37247/pabs.1.2020.7 · Cited by 1
Rodriguez, L., Jacques, C., & Ory, B. (2014) · Elsevier eBooks · doi:10.1016/b978-0-12-416721-6.00015-7 · Cited by 1
Release of MicroRNA‐Containing Vesicles Can Stimulate Angiogenesis and Metastasis in Renal Carcinoma
Collino, F., Grange, C., & Camussi, G. (2013) · doi:10.1002/9781118300312.ch37 · Cited by 1
Cell Type-Specific Effects of miR-21 Loss Attenuate Tumor Progression in MYC-Driven Prostate CancerPreprint
Zennami, K., Graham, M. K., Chikara, S., Sysa‐Shah, P., Rafiqi, F., Wang, R., Abel, B., Zeng, Q., Krueger, T. E. G., Brennen, W. N., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.05.14.654101 · Cited by 2
Involvement of MicroRNAs in Human Cancer: Discovery and Expression Profiling
Negrini, M., & Călin, G. A. (2009) · Springer eBooks · doi:10.1007/978-90-481-2675-0_5
Regulation of molecular processes in diffuse large b-cell lymphoma
Högfeldt, T. (2013) · Figshare
MicroRNA and Glial Tumors: Tiny Relation with Great Potential
Šáňa, J., Hajdúch, M., & Slabý, O. (2012) · InTech eBooks · doi:10.5772/22941
“Consequently, down-regulation of miR-21 decreased migratory and invasive abilities in glioma cells (Gabriely et al., 2008).”
BackgroundmiRNAs in Cancer Invasion and Metastasis
Humphries, B. A., & Yang, C. (2013) · Wiley eBooks · doi:10.1002/9781118695999.ch8
Reis, S. T. (2011) · Digital Library of Theses and Dissertations (Universidade de São Paulo) · doi:10.11606/t.5.2011.tde-22092011-133255
MicroRNA Gene Regulatory Networks in Peripheral Nerve Sheath Tumors
Subramanian, S. (2012) · Defense Technical Information Center (DTIC) · doi:10.21236/ada573825
MicroRNA Adjuvants in Stem Cell‐Based Cancer Therapy
Anderegg, M. C. J., & Corsten, M. F. (2013) · Wiley eBooks · doi:10.1002/9781118660423.ch15
MicroRNAs Regulated Brain Tumor Cell Phenotype and Their Therapeutic Potential
Zhang, C., Chen, B., Xu, X., Han, B., Wang, G., & Wang, J. (2013) · InTech eBooks · doi:10.5772/52362
“Mir-21 knockdown decreases RECK and TIMP3 protein levels and MMPs activity both in vivo and in vitro leading to a reduction of glioma cell motility and invasion [43].”
BackgroundMellios, N. (2009) · The Journal of the American Medical Association (JAMA) Network (American Medical Association) · doi:10.13028/pz41-4991
“These range from examples of miRNAs that can act as oncogenes (Gabriely et al., 2008) or onco-suppressors (Cimmino et al.”
Background
Metadata
- Authors
- Gabriely, G., Wurdinger, T., Kesari, S., Esau, C. C., Burchard, J., Linsley, P. S., & Krichevsky, A. M.
- Affiliations
- Brigham and Women's Hospital (US)
- Harvard University (US)
- Regulus Therapeutics (United States) (US)
- Corresponding author
- Krichevsky, Anna M.
- ORCID
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 2008-09-01
- Volume
- 28
- Issue
- 17
- Pages
- 5369-5380
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- PMC
- PMC2519720
- OpenAlex
- W2163655902
- Cited by
- 888
- References
- 62
- Citations by year
- 2026: 13 · 2025: 19 · 2024: 21 · 2023: 29 · 2022: 20 · 2021: 21 · 2020: 43 · 2019: 41 · 2018: 33 · 2017: 56 · 2016: 56 · 2015: 75 · 2014: 76 · 2013: 86 · 2012: 91
- FWCI
- 21.02
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular and Cellular Biology (publishedVersion)
- PubMed (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
- PubMed Central (submittedVersion)
- Pure Amsterdam UMC (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- National Institutes of Health (CA86355)
- National Cancer Institute (R21 CA116141, P50 CA86355-04, P50CA086355)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Protease and Inhibitor Mechanisms
- Health Sciences › Medicine › Oncology › Glioma Diagnosis and Treatment
- Keywords
- miR-21, glioma invasion, glioblastoma, matrix metalloproteinases, RECK, TIMP-3, matrix metalloproteinase inhibitors, cell migration, apoptosis, antisense oligonucleotides, microRNA inhibition, tumor malignancy
- MeSH terms
- Animals, Base Sequence, Cell Movement, Enzyme Inhibitors, Extracellular Matrix, Glioma, Humans, Molecular Sequence Data, Neoplasm Invasiveness, Neoplasm Transplantation, RNA, Messenger, Down-Regulation, Gene Expression Regulation, Neoplastic, Apoptosis, Disease Progression, Oligonucleotide Array Sequence Analysis, Matrix Metalloproteinases, Gene Expression Profiling, MicroRNAs, Cell Line, Tumor, Mice, Genes, Neoplasm, Matrix Metalloproteinase Inhibitors
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-19, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-19 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
