Exosomal miR-21-5p from glioma associated mesenchymal stem cells promotes the progression and glycolysis of glioblastoma via PDHA1
Open accessAbstract
Glioblastoma (GBM) is highly malignant and grows rapidly, and there is currently a lack of effective treatments. Metabolism provides the basis for the occurrence and development of GBM. Pyruvate dehydrogenase A1 (PDHA1) is a key component in both the tricarboxylic acid cycle and glycolysis, playing an important role in the metabolic processes related to cancer, but its role in GBM remains unclear. Glioma associated mesenchymal stem cells (GaMSC) play a significant role in the development of glioma. This study aims to explore the relationship between GaMSC derived exosomes (GAMSC-EXO) and PDHA1, as well as the effects and mechanisms on GBM glucose metabolism. In this study, human GaMSC-derived exosomes were isolated and identified. The role of GAMSC-EXO in GBM proliferation, migration, invasion and glucose metabolism was investigated. The upstream miRNA of PDHA1 was predicted and the relationship between miR-21-5p and PDHA1 in GAMSC-EXO and its effect on GBM glucose metabolism was investigated. We found that GAMSCs promote GBM cell proliferation, migration, invasion and glycolysis by releasing exosomes. After inhibiting GBM glycolysis, GBM proliferation, migration and invasion abilities were weakened. MiR-21-5p in exosomes was identified as the miRNA that affects the above biological behaviors. Mechanismly, miR-21-5p directly binds to the mRNA of PDHA1 and downregulates its transcription, thereby promoting GBM glycolysis. Together, this study demonstrated that exosomal miR-21-5p from GAMSC promoted GBM proliferation, migration, invasion, and glycolysis by targeting PDHA1, which provided novel insights into the metabolic interactions between GAMSCs and GBM cells, emphasizing the importance of exosome-mediated communication in tumor progression.
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Written from the paper’s full text.
TL;DR
Glioma-associated mesenchymal stem cell (GAMSC)-derived exosomes promote glioblastoma (GBM) proliferation, migration, invasion, and glycolysis. Exosomal miR-21-5p directly targets PDHA1 and downregulates it, linking GAMSC-to-GBM communication to metabolic reprogramming.
Key findings
- GAMSCs were positive for CD73 (99.3%), CD90 (93.9%), and CD44 (91.6%), and negative for hematopoietic markers (5.2% negative cocktail); GAMSC-derived conditioned medium and exosomes increased GBM proliferation, migration, and invasion.
- GAMSC-EXO enhanced glycolysis in GBM cells, increasing PKM2 expression, glucose utilization, lactate production, intracellular ATP, OCR, basal/maximal respiration, and ECAR; the glycolysis inhibitor 2-DG partially inhibited GAMSC-EXO-promoted proliferation and invasion.
- miR-21-5p was identified as a direct repressor of PDHA1: luciferase activity was reduced by miR-21-5p mimics and increased by inhibitor with wild-type PDHA1 3′UTR, but no difference was seen with mutant PDHA1 reporters.
- In vivo, GAMSC-EXO increased tumor fluorescence, shortened survival (Kaplan–Meier, P < 0.05), and increased PKM2 expression by IHC/IF; PDHA1 knockdown increased glucose utilization, lactate production, ATP, OCR, and ECAR in GBM cells.
Methods
- U87 and U251 GBM cells and GAMSCs were cultured; GAMSCs were transfected with miR-21-5p mimics, inhibitor, or controls, and GBM cells with siPDHA1 or control.
- Exosomes were isolated from GAMSC conditioned medium by differential centrifugation/ultracentrifugation and characterized by TEM, nanoparticle size, western blot (TSG101, CD81, calnexin), and PKH26 uptake.
- Functional assays included colony formation, MTT, wound healing, Transwell, glucose/lactate/ATP measurements, OCR/ECAR, dual-luciferase reporter assays, RT-PCR, western blot, and an orthotopic nude mouse model with survival analysis and IHC/IF for PKM2.
Limitations
- The paper states it only focused on the effect of GAMSC-EXO on GBM cell glycolysis and did not explain whether GAMSC-related changes in the tumor microenvironment (immunity, angiogenesis) are caused by GAMSC extracellular vesicles.
- The paper states that effects of extracellular vesicles from other cell sources, and what drives these cell-to-cell interactions in GBM progression, require further exploration.
- Evident from the text: some reported details are inconsistent or typographical (e.g., “miR-221 inhibitors” in the miR-21-5p transfection-efficiency description, and an MTT comparison sentence that appears to compare CM with CM), which limits clarity.
Model-written summary. Check it against the paper before relying on it.
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Statistics
Claims the paper makes
- Findingown data
GAMSC-EXO promotes GBM cell migration.
“The results of Transwell assay indicated that EXO could promote GBM cell migration and invasion (Fig. 3F and G).”
- Also stated in: § GAMSC-EXO promotes GBM cell proliferation, migration and invasion · hedged
“The results revealed that GAMSC-EXO could promotes GBM cell migration, invasion and proliferation.”
Quote in the paperSubstantial claim - Also stated in: § GAMSC-EXO promotes GBM cell proliferation, migration and invasion · hedged
- Findingown data
GAMSC-EXO promotes glycolysis in GBM cells.
“The results showed that GAMSC-EXO could promote the expression of PKM2 at both protein and gene levels (Fig. 4A and B).”
- Also stated in: § GAMSC-EXO promotes glycolysis in GBM cells · hedged
“GAMSC-EXO could promote the glucose utilization, lactate production and intracellular ATP levels in GBM cells.”
- Also stated in: § GAMSC-EXO promotes glycolysis in GBM cells · hedged
“Together, these results suggested that GAMSC-EXO enhanced glycolysis in GBM cells.”
Quote in the paperSubstantial claim - Also stated in: § GAMSC-EXO promotes glycolysis in GBM cells · hedged
- Findingown data
GAMSC-EXO promotes GBM cell proliferation.
“The clone formation assay results indicated that the quantity of cell proliferation in the BM + EXO group was markedly increased in comparison to the BM group (Fig. 3D).”
- Also stated in: § GAMSC-EXO promotes GBM cell proliferation, migration and invasion · plain
“The MTT results showed that from 0 to 72 h, the value of BM + EXO group at 490 nm is significantly higher than that of CM group (Fig. 3E).”
- Also stated in: § GAMSC-EXO promotes GBM cell proliferation, migration and invasion · hedged
“The results revealed that GAMSC-EXO could promotes GBM cell migration, invasion and proliferation.”
Quote in the paperSubstantial claim - Also stated in: § GAMSC-EXO promotes GBM cell proliferation, migration and invasion · plain
- Findingown data
GAMSC-derived conditioned medium promotes GBM cell migration.
“The results of Transwell assay indicated that CM could promote GBM cell migration and invasion (Fig. 2C and D).”
- Also stated in: § GAMSC-derived conditioned medium promotes GBM cell proliferation, migration, and invasion · plain
“In addition, the wound healing assay also verified that CM from GAMSC could promote GBM cell migration (Fig. 2E).”
Quote in the paperSubstantial claim - Also stated in: § GAMSC-derived conditioned medium promotes GBM cell proliferation, migration, and invasion · plain
- Findingown data
Inhibition of glycolysis with 2-DG inhibits GAMSC-EXO-induced GBM cell invasion.
“the influence of GAMSC-EXO on enhancing the invasion of GBM cells could be inhibited by 2-DG (Figure s1C).”
Quote in the paperSubstantial claim
- Findingown data
GAMSC-EXO treatment decreases PDHA1 expression in GBM cells.
“GAMSC-EXO treatment significantly decreased the PDHA1 expression level in GBM cells (Fig. 6A and B).”
Quote in the paperSubstantial claim - Findingown data
Inhibition of glycolysis with 2-DG partially inhibits GAMSC-EXO-induced GBM cell proliferation.
“GAMSC-EXO can promote GBM cell proliferation, but this effect can be partially inhibited by 2-DG.”
- Also stated in: § GAMSC-EXO promotes glycolysis in GBM cells · plain
“2-DG can inhibit the proliferative effect of GAMSC-EXO on GBM cells (Figure s1B).”
Quote in the paperSubstantial claim - Also stated in: § GAMSC-EXO promotes glycolysis in GBM cells · plain
- Findingown data
GAMSC-EXO promotes GBM growth in vivo.
“the fluorescence intensity of the GAMSC-EXO group was markedly higher than that of the NC (three replicate samples in each group).”
- Also stated in: § GAMSC-EXO can promote GBM growth and glycolysis in vivo · boosted
“The above results demonstrated that GAMSC-EXO could promote the growth of GBM and accelerated host death.”
Quote in the paperSubstantial claim - Also stated in: § GAMSC-EXO can promote GBM growth and glycolysis in vivo · boosted
- Findingown data
GAMSC-EXO enhances PKM2 expression in vivo.
“the expression of PKM2 in the GAMSC-EXO group was increased in comparison to the NC (Fig. 5E and F)”
- Also stated in: § GAMSC-EXO can promote GBM growth and glycolysis in vivo · hedged
“GAMSC-EXO could enhance the expression of PKM2 in vivo.”
Quote in the paperSubstantial claim - Also stated in: § GAMSC-EXO can promote GBM growth and glycolysis in vivo · hedged
- Findingown data
GAMSC-EXO miR-21-5p promotes glycolysis in GBM cells.
“GAMSC-EXO miR-21-5p mimics group (mimics) had a higher glucose utilization, lactate production and intracellular ATP levels, whereas those of the GAMSC-EXO miR-21-5p inhibitor group (inhibitor) were lower.”
- Also stated in: § GAMSC-EXO miR-21-5p promotes glycolysis in GBM cells · hedged
“The above results indicated that GAMSC-EXO miR-21-5p could enhance glycolysis in U87 cells.”
- Also stated in: § GAMSC-EXO miR-21-5p promotes glycolysis in GBM cells · hedged
“GAMSC-EXO miR-21-5p could also enhance glycolysis in U251 cells (Figure S2).”
Quote in the paperSubstantial claim - Also stated in: § GAMSC-EXO miR-21-5p promotes glycolysis in GBM cells · hedged
- Findingown data
GAMSC-EXO enhances glycolytic flux in GBM cells.
“cells in the GAMSC-EXO group exhibited enhanced glycolytic flux.”
- Also stated in: § GAMSC-EXO promotes glycolysis in GBM cells · plain
“the detected intermediates of glycolytic flux were also increased in the GAMSC-EXO group in comparison to the NC group (Figure s3 D-G).”
Quote in the paperSubstantial claim - Also stated in: § GAMSC-EXO promotes glycolysis in GBM cells · plain
- Findingown data
GAMSC-EXO are taken up by GBM cells.
“PKH26-labeled GAMSC-EXO were localized in the cytoplasm of GBM cells (Fig. 3C).”
Quote in the paperSubstantial claim - Findingown data
GAMSC-derived conditioned medium promotes GBM cell invasion.
“The results of Transwell assay indicated that CM could promote GBM cell migration and invasion (Fig. 2C and D).”
Quote in the paperSubstantial claim - Findingown data
GAMSC-EXO promotes GBM cell invasion.
“The results of Transwell assay indicated that EXO could promote GBM cell migration and invasion (Fig. 3F and G).”
Quote in the paperSubstantial claim - Findingown data
GAMSC-EXO shortens survival time in a GBM mouse model.
“survival analysis (Kaplan–Meier) in Fig. 5D showed that the survival time of the GAMSC-EXO group was significantly shorter in comparison to NC group.”
Quote in the paperSubstantial claim - Findingown data
GAMSC-derived conditioned medium promotes GBM cell proliferation.
“The clone formation assay findings revealed that the rate of cell proliferation in the CM group was markedly increased in comparison to the basal medium (BM) group (Fig. 2A).”
- Also stated in: § GAMSC-derived conditioned medium promotes GBM cell proliferation, migration, and invasion · plain
“The MTT results showed that from 0 to 72 h, the value of CM group at 490 nm is significantly higher than that of CM group (Fig. 2B).”
Quote in the paperSubstantial claim - Also stated in: § GAMSC-derived conditioned medium promotes GBM cell proliferation, migration, and invasion · plain
- Findingown data
GAMSC-EXO miR-21-5p inhibits PDHA1 expression in GBM cells.
“GAMSC-EXO miR-21-5p could inhibit the PDHA1 expression in GBM cells (Fig. 7F).”
Quote in the paperSubstantial claim - Findingown data
The isolated cells were GAMSCs.
“Together, the above results show that we have successfully extracted GAMSC.”
- Also stated in: § Identification of Glioma associated mesenchymal stem cells (GAMSC) · plain
“Flow cytometry results showed that these cells were positive for the MSC markers CD73(99.3%), CD90(93.9%), and CD44 (91.6%), and were negative for the hematopoietic stem cell markers CD45, CD34, and HLA-DR (5.2%, mixed as a negative cocktail) (Fig. 1B).”
Quote in the paperSubstantial claim - Also stated in: § Identification of Glioma associated mesenchymal stem cells (GAMSC) · plain
- Findingown data
Knockdown of PDHA1 promotes glycolysis in GBM cells.
“compared with the NC group, the glucose utilization rate, lactate production rate and ATP level in cells were significantly increased in the PDHA1 knockdown group (siPDHA1).”
- Also stated in: § Knockdown of PDHA1 can promote glycolysis in GBM cells · plain
“the OCR of the mitochondrial oxidative respiration phase in siPDHA1 group was significantly increased, and basal respiration and maximum respiration were also enhanced in comparison to the NC (Fig. 6H and I).”
- Also stated in: § Knockdown of PDHA1 can promote glycolysis in GBM cells · plain
“the results of ECAR were similar with the OCR results.”
Quote in the paperSubstantial claim - Also stated in: § Knockdown of PDHA1 can promote glycolysis in GBM cells · plain
- Interpretationreasoning
GAMSC-EXO directly provides miR-21-5p to GBM.
“GAMSC-EXO directly provides miR-21-5p to GBM, which explains why GAMSC promotes GBM malignancy from the perspective of cell–cell interaction.”
Quote in the paperSubstantial claim - Interpretationown data
GAMSC-EXO promotes GBM cell invasion and proliferation by enhancing glycolysis.
“The above results demonstrated that GAMSC-EXO was able to promote the invasion and proliferation of GBM cells by enhancing glycolysis.”
Quote in the paperSubstantial claim - Interpretationown data
miR-21-5p in GAMSC-EXO is the miRNA that affects GBM proliferation, migration, invasion, and glycolysis.
“MiR-21-5p in exosomes was identified as the miRNA that affects the above biological behaviors.”
Quote in the paperSubstantial claim
- May combine two claims. 3
May combine two claims.
Findingown dataThe isolated exosomes from GAMSC conditioned medium are exosomes (express TSG101 and CD81, lack calnexin, round/elliptical).
“The nanoparticle size profile and the transmission electron microscopy showed that the isolated exosomes were round or elliptical membranous vesicles with clear margins (Fig. 3A).”
- Also stated in: § GAMSC-EXO promotes GBM cell proliferation, migration and invasion · plain
“The western blot results showed that the exosomes expressed the marker proteins TSG101 and CD81 and lacked the endoplasmic reticulum protein calnexin (Fig. 3B).”
Quote in the paperSubstantial claim- Also stated in: § GAMSC-EXO promotes GBM cell proliferation, migration and invasion · plain
May combine two claims.
Interpretationown datamiR-21-5p directly binds the 3'UTR of PDHA1 and negatively regulates its mRNA levels in GBM cells.
“This result indicated that miR-21-5p could directly bind the 3’UTR sequence of PDHA1 and negatively regulate its mRNA levels in GBM cells.”
- Also stated in: § Identifying miR-21-5p from GAMSC-EXO as a direct repressor of PDHA1 · plain
“miR-21-5p was identified as a direct repressor of PDHA1 in GAMSC-EXO.”
Quote in the paperSubstantial claim- Also stated in: § Identifying miR-21-5p from GAMSC-EXO as a direct repressor of PDHA1 · plain
May combine two claims.
Interpretationown dataExosomal miR-21-5p from GAMSC promotes GBM proliferation, migration, invasion, and glycolysis by targeting PDHA1.
“Together, this study demonstrated that exosomal miR-21-5p from GAMSC promoted GBM proliferation, migration, invasion, and glycolysis by targeting PDHA1”
- Also stated in: § Discussion · boosted
“Together, this study demonstrated that GAMSCs provide miR-21-5p to GBM by secreting exosomes, thereby reducing the expression level of PDHA1 in GBM, promoting GBM glycolysis and cancer cell phenotypes such as proliferation and invasion.”
Quote in the paperSubstantial claim- Also stated in: § Discussion · boosted
The paper relies on this without support.
The role and mechanism of PDHA1 in GBM remain unclear.
“but its role in GBM remains unclear.”
“But its role and mechanism in GBM remain unclear.”
The paper relies on this without support.
The mode of action by which GAMSC affects GBM malignancy is unclear.
“Although the effect of GAMSC on the malignancy of GBM has been reported, its mode of action is still unclear and needs further exploration.”
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.
Conditioned-medium group is compared with itself
MinorThe results say the CM group's MTT value was significantly higher than the CM group's own value. The figure caption instead identifies BM as the comparison group.
“The MTT results showed that from 0 to 72 h, the value of CM group at 490 nm is significantly higher than that of CM group (Fig. 2B).”
“(B) MTT assay results of GBM cells with BM or CM. *P < 0.05 vs. BM.”
Fig. 7 transfection reagent is identified as both miR-21 and miR-221
MinorThe results describe transfecting GAMSC with miR-21-5p mimics and inhibitors, but the Fig. 7E caption calls them miR-221 mimics and inhibitors. This leaves the identity of the reagents used for that result inconsistent.
“we transfected GAMSC with miR-21-5p mimics/inhibitors and its negative control miR-21-5p mimics/inhibitors-NC”
“(E) RT-PCR results: Transfection efficiency of miR-221 mimics and inhibitors.”
Differentiation stains are assigned to different outcomes
MinorThe results assign Alizarin Red S to osteogenic differentiation and Oil Red O to adipogenic differentiation, while the Fig. 1 caption assigns them to lipogenic and osteogenic differentiation, respectively.
“Alizarin Red S, Oil Red O, and Alcian Blue staining showed that the isolated cells were induced to undergo osteogenic, adipogenic, and chondrogenic differentiation (Fig. 1C).”
“(C) Representative graph of Alizarin Red S, Oil Red O, or Alcian Blue staining assays of GAMSC lipogenic, osteogenic, and chondrogenic differentiation ability, (Bar = 50 μm).”
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Works this paper cites that were later retracted, from the retraction notices publishers deposit. Major when the notice came out before this paper was published.
Cites a retracted work: 10.18632/oncotarget.10782
InfoThe cited work was retracted on 2025-11-06 (notice 10.18632/oncotarget.28777), not before this paper was published (2025-01-17).
Cited work 10.18632/oncotarget.10782 · retracted 2025-11-06 · notice 10.18632/oncotarget.28777 · this paper published 2025-01-17
“Li, Y. et al. PDHA1 gene knockout in prostate cancer cells results in metabolic reprogramming towards greater glutamine dependence. Oncotarget 7(33), 53837–53852 (2016).”
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Zhang, Q., Xiang, W., Xue, B., Yi, D., Zhao, H., & Fu, P. (2021) · Oncology Letters · doi:10.3892/ol.2021.12476 · Cited by 16 · see citing works
Self-citationExtracellular Vesicles Involvement in the Modulation of the Glioblastoma Environment
Ciccocioppo, F., Lanuti, P., Marchisio, M., & Miscia, S. (2020) · Journal of Oncology · doi:10.1155/2020/3961735 · Cited by 13 · see citing works
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Cited by
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The tumor microenvironment: adding pieces to the puzzle
Aguilar‐Cázares, D., Perez-Medina, M., Benito-Lopez, J. J., Galicia-Velasco, M., Meneses-Flores, M., Camarena, Á., & López-González, J. S. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1731338 · Cited by 13 · see citing works
“Notably, recent studies indicate that exosomal miR-21-5p also targets PDHA1 to promote glycolysis in glioblastoma, directly linking vesicle-mediated communication with metabolic reprogramming and the Warburg effect (164).”
Ramezani, A., Rahnama, M., Mahmoudian, F., Shirazi, F., Ganji, M., Bakhshi, S., Khalesi, B., Hashemi, Z. S., & Khalili, S. (2025) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-025-10204-7 · Cited by 4 · see citing works
Comprehensive pan-cancer analysis of USP35 and validation of its role in gastric cancer
Yan, L., Zhang, Y., Zhang, Y., et al. (2025) · Human Genomics · doi:10.1186/s40246-025-00850-6 · Cited by 3 · see citing works
Self-citationFanglei, C. H. A. I., Liu, C., Liu, Y., & Zou, W. (2025) · Frontiers in Neurology · doi:10.3389/fneur.2025.1678595 · Cited by 3 · see citing works
“This finding suggests the possibility that succinate may utilize analogous extracellular transport pathways (34, 35).”
Muraleedharan, A., Rangavajhula, K., & Ray, S. K. (2026) · Cells · doi:10.3390/cells15050422 · Cited by 2 · see citing works
Zang, Y., & Zhao, R. (2026) · Journal of Hepatocellular Carcinoma · doi:10.2147/jhc.s580617 · Cited by 1 · see citing works
Dong, W., Wei, H., Duan, L., Hu, H., & Zhao, M. (2025) · Oncology and Translational Medicine · doi:10.1097/ot9.0000000000000115
Glycolytic Signaling Pathways and Anti‐Glycolytic Therapy for Cancer: Research and Perspectives
Li, X., Li, S., Li, D. K. T., Xi, Y., Gu, Q., Liu, J., Hou, S., Zhang, X., Jin, C., Yang, M., et al. (2026) · Comprehensive physiology · doi:10.1002/cph4.70177
“In addition to facilitating immune evasion, glycolysis also enhances the proliferation and metastasis of tumor cells (Liu, Liu, et al. 2025; Zhang, Lv, et al. 2025).”
MicroRNA‐3651 Facilitates Glioma Progression by Targeting SCN3B and Serves as a Prognostic Indicator
Wang, J., Deng, Y., Nie, D., et al. (2026) · Acta Neurologica Scandinavica · doi:10.1155/ane/7350637
- Authors
- Zhang, Y., Lv, P., Zhang, Q., Xiang, W., Jiang, X., Guo, Z., & Zhang, T.
- Affiliations
- Huazhong University of Science and Technology (CN)
- Wuhan Union Hospital (CN)
- Wuhan University (CN)
- Corresponding author
- Jiang, Xiaobing
- Guo, Zijun
- Zhang, Tao
- Venue
- Scientific Reports
- Published
- 2025-01-17
- Volume
- 15
- Issue
- 1
- Pages
- 2320-2320
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC11747265
- OpenAlex
- W4406597812
- Semantic Scholar
- dd4f5f89de70e7aba07ebdbdf10d6846b9c7044f
- Cited by
- 9
- References
- 36
- Citations by year
- 2026: 5 · 2025: 4
- FWCI
- 2.25
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Scientific Reports (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- PubMed Central (submittedVersion, cc-by-nc-nd)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (82273210, 82403222, 82200972)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Extracellular vesicles in disease
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Health Sciences › Medicine › Genetics › Glioma Diagnosis and Treatment
- Keywords
- glioblastoma, exosomes, miR-21-5p, PDHA1, glycolysis, tumor glucose metabolism, tumor cell proliferation, cell migration and invasion, exosome-mediated intercellular communication, tumor microenvironment
- MeSH terms
- Animals, Brain Neoplasms, Cell Movement, Glioblastoma, Glioma, Glucose, Glycolysis, Humans, Gene Expression Regulation, Neoplastic, Disease Progression, Pyruvate Dehydrogenase (Lipoamide), MicroRNAs, Cell Line, Tumor, Cell Proliferation, Mice, Exosomes, Mesenchymal Stem Cells
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.
Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-21.
Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-21.
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.
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