Frequent loss of PDCD4 expression in human glioma: Possible role in the tumorigenesis of glioma
Open accessAbstract
Programmed cell death 4 (PDCD4) was recently identified as a novel tumor suppressor gene. The loss of PDCD4 expression was found in several types of human cancer cell lines. To date, however, the status of PDCD4 expression in human glioma tissue is not known. In the present study, the expression of PDCD4 in 30 glioma samples was determined at both mRNA and protein levels by means of RT-PCR, Western blotting, and immunohistochemistry. Herein, we demonstrate, for the first time, that 47% (14/30) of glioma samples lost the expression of PDCD4 mRNA, and 77% (23/30) of glioma samples lacked the PDCD4 protein expression, whereas adjacent normal glial tissues expressed high levels of PDCD4 mRNA and protein. Furthermore, the loss of PDCD4 expression does not significantly correlate with the pathological and clinical features of the glioma. Our new data suggest that the loss of PDCD4 expression is a frequent event in human glioma and may partially contribute to the development of the tumor.
AI snapshot
Written from the paper’s full text.
TL;DR
This study reports frequent loss of PDCD4 expression in human glioma at both mRNA and protein levels compared with adjacent normal glial tissue. The authors suggest this loss may contribute to glioma tumorigenesis, though it did not significantly correlate with tumor grade or histological type.
Key findings
- PDCD4 mRNA was lost in 47% (14/30) of glioma samples, while 12 of the remaining 16 samples showed reduced PDCD4 mRNA compared with three normal adjacent brain tissue controls.
- PDCD4 protein was absent in 77% (23/30) of gliomas by Western blotting and immunohistochemistry; the other 6 showed weak PDCD4 bands.
- Adjacent normal glial tissues expressed high levels of PDCD4 mRNA and protein, whereas the glioma cell line U251 lacked PDCD4 expression.
- Loss of PDCD4 expression showed no significant correlation with sex, age, tumor size, tumor grade, or histological type.
Methods
- Glioma specimens were obtained from 30 patients aged 40–60 years (mean 50 years) who underwent surgery; three normal glial tissues were acquired from tumor-adjacent tissue, and the U251 glioma cell line was also used.
- PDCD4 expression was assessed at mRNA level by semiquantitative RT-PCR and at protein level by Western blotting and immunohistochemistry.
- Statistical analysis used the χ² test to examine correlation between PDCD4 protein expression and pathological features, with p<0.05 considered significant.
Limitations
- The authors state that the precise mechanism by which PDCD4 expression affects glioma tumorigenesis needs further investigation in a large set of patient samples.
- The authors note that the molecular basis for the PDCD4 expression pattern is unclear.
- Evident from the text: the study is small (30 glioma samples and only 3 normal glial controls), relies on semiquantitative expression assays, and does not include functional experiments to establish causality.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
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Cites
Statistics
Claims the paper makes
0 of 14 cited sources checked · 0 supported · 0 flagged
- Findingown data
Adjacent normal glial tissues expressed high levels of PDCD4 mRNA and protein.
“whereas adjacent normal glial tissues expressed high levels of PDCD4 mRNA and protein.”
- Also stated in: § Lacking or decreased expression of PDCD4 mRNA in gliomas. · plain
“all of three normal brain tissues adjacent to the tumor lesion expressed a high level of PDCD4 mRNA”
- Also stated in: § High frequent loss of PDCD4 protein expression in gliomas. · plain
“normal brain tissues adjacent to tumor, which showed strong PDCD4 expression”
Quote in the paperSubstantial claim - Also stated in: § Lacking or decreased expression of PDCD4 mRNA in gliomas. · plain
- Findingown data
In 30 glioma specimens, 23 (77%) lacked PDCD4 protein expression.
“77% (23/30) of glioma samples lacked the PDCD4 protein expression”
- Also stated in: § High frequent loss of PDCD4 protein expression in gliomas. · plain
“In 30 cases of the gliomas, 23 (77%) exhibited no relevant PDCD4 bands and the other 6 showed weak PDCD4 bands, compared with normal brain tissues adjacent to tumor, which showed strong PDCD4 expression (Fig. 2).”
Quote in the paperSubstantial claim - Also stated in: § High frequent loss of PDCD4 protein expression in gliomas. · plain
- Findingown data
There was no significant relationship between loss of PDCD4 expression and tumor grade or histological type.
“Unexpectedly there was also no significant relationship between loss of PDCD4 expression and tumor grade or histological type (Fig. 4).”
Quote in the paperSubstantial claim - Findingown data
Loss of PDCD4 expression does not significantly correlate with the pathological and clinical features of glioma.
“Furthermore, the loss of PDCD4 expression does not significantly correlate with the pathological and clinical features of the glioma.”
- Also stated in: § High frequent loss of PDCD4 protein expression in gliomas. · plain
“The loss of PDCD4 in gliomas had no significant relationships with tumor grade or histological type.”
Quote in the paperSubstantial claim - Also stated in: § High frequent loss of PDCD4 protein expression in gliomas. · plain
- Findingown data
No PDCD4 expression was observed in the glioma cell line U251.
“no PDCD4 expression was observed in the glioma cell line (U251)”
Quote in the paperNot a substantial claim
- Findingown data
There was no significant correlation of lack of PDCD4 expression with sex, age, and tumor size.
“As expected, there was no significant correlation of lack of PDCD4 expression with sex, age, and tumor size (data not shown).”
Quote in the paperNot a substantial claim - Findingown data
The loss of PDCD4 proteins was more than that of PDCD4 mRNA.
“The data from Western blot experiment showed that the loss of PDCD4 proteins was more than that of PDCD4 mRNA (Table I).”
Quote in the paperSubstantial claim - Findingown data
In 30 glioma specimens, 14 (47%) lost PDCD4 mRNA expression.
“47% (14/30) of glioma samples lost the expression of PDCD4 mRNA”
- Also stated in: § Lacking or decreased expression of PDCD4 mRNA in gliomas. · plain
“In 30 glioma specimens, 14 (47%) lost PDCD4 mRNA expression (Table I).”
Quote in the paperSubstantial claim - Also stated in: § Lacking or decreased expression of PDCD4 mRNA in gliomas. · plain
- Findingown data
PDCD4 expression is higher in normal tissue (tumor adjacent tissue) than in tumor tissue for the paired tumor sample by immunohistochemistry.
“Our results show that PDCD4 expression is higher in the normal tissue, i.e. tumor adjacent tissue, than the tumor tissue for the paired tumor sample by immunohistochemistry.”
Quote in the paperSubstantial claim - Findingown data
Some gliomas expressed PDCD4 mRNA but not PDCD4 protein.
“Noteworthily, some gliomas such as sample 5 expressed PDCD4 mRNA but not PDCD4 protein.”
Quote in the paperSubstantial claim - Premisecitation
PDCD4 acts as a novel tumor suppressor gene.
“Programmed cell death 4 (PDCD4) was recently identified as a novel tumor suppressor gene.”
- Also stated in: § Introduction · boosted
“thereby confirming that PDCD4 acts as a novel tumor suppressor gene.”
- Also stated in: § Discussion · boosted
“Previous study of mammalian cell lines has confirmed that PDCD4 acts as a novel tumor suppressor gene (12,(18)(19)(20)(21)(22)(23)(24).”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [6]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [7]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [8]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Also stated in: § Introduction · boosted
- Premisecitation
PDCD4 is expressed ubiquitously in human normal tissues.
“It is expressed ubiquitously in human normal tissues, whereas loss of its expression is found in several types of human cancer cell lines (13), and in primary lung cancer (14) and in primary pancreatic cancer (15).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [13]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Interpretationown data
Loss or absence of PDCD4 expression may contribute to the development or tumorigenesis of glioma.
“Our new data suggest that the loss of PDCD4 expression is a frequent event in human glioma and may partially contribute to the development of the tumor.”
- Also stated in: § Discussion · hedged
“our results indicate that loss or absence of PDCD4 expression may play a crucial role in the pathogenesis of glioma, maybe via downregulation of apoptosis.”
- Also stated in: § Discussion · hedged
“our new results suggest that loss or absence of PDCD4 expression may be a key factor in the tumorigenesis of glioma.”
Quote in the paperSubstantial claim - Also stated in: § Discussion · hedged
- Interpretationown data
Loss of PDCD4 expression is a frequent event in human glioma.
“Our new data suggest that the loss of PDCD4 expression is a frequent event in human glioma and may partially contribute to the development of the tumor.”
- Also stated in: § Discussion · boosted
“we clearly demonstrate, for the first time, that high frequent loss of PDCD4 expression exists in primary gliomas”
Quote in the paperSubstantial claim - Also stated in: § Discussion · boosted
- Interpretationown data
Loss of PDCD4 expression in certain gliomas might occur after mRNA transcription.
“These suggested that loss of PDCD4 expression in certain gliomas might occur after mRNA transcription.”
Quote in the paperSubstantial claim - Premisecitation
PDCD4 inhibits tumor promoter-induced transformation in the mouse JB6 model system.
“Indeed, the following studies demonstrated that PDCD4 was able to inhibit tumor promoter-induced transformation in the mouse JB6 model system (6)(7)(8), thereby confirming that PDCD4 acts as a novel tumor suppressor gene.”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [6]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [7]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [8]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Classified as probably not a substantial claim. 13
Probably not a substantial claim: may not pass S3 (load-bearing).
Findingown dataPositive PDCD4 staining localized in cytoplasm.
“In addition, Fig. 3 showed that the positive PDCD4 staining localized in cytoplasm.”
Quote in the paperNot a substantial claimClassified as probably not a substantial claim.
Study design and conductreasoningNo patient had received adjuvant immunosuppressive treatment including radiotherapy or chemotherapy prior to surgery.
“No patient had received adjuvant immunosuppressive treatment including radiotherapy or chemotherapy prior to surgery in order to eliminate the variable from affecting gene expression.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationLoss of PDCD4 expression is found in primary lung cancer.
“It is expressed ubiquitously in human normal tissues, whereas loss of its expression is found in several types of human cancer cell lines (13), and in primary lung cancer (14) and in primary pancreatic cancer (15).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [14]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Probably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductnone givenThe pathological analysis was according to World Health Organization (WHO) criteria.
“The pathological analysis was according to World Health Organization (WHO) criteria.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductnone givenRT-PCR was performed at least twice in independent experiments.
“The RT-PCR was performed at least twice in independent experiments.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductnone givenHuman beta-actin was amplified as an internal control from parallel samples.
“Human ß-actin was amplified as an internal control from parallel samples.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductnone givenAll slides were independently analyzed by two pathologists.
“All of the slides were independently analyzed by two pathologists.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationLoss of PDCD4 expression is found in several types of human cancer cell lines.
“It is expressed ubiquitously in human normal tissues, whereas loss of its expression is found in several types of human cancer cell lines (13), and in primary lung cancer (14) and in primary pancreatic cancer (15).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [13]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Probably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductnone givenWestern blotting was performed at least twice in independent experiments.
“Western blotting was performed at least twice in independent experiments.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationLoss of PDCD4 expression is found in primary pancreatic cancer.
“It is expressed ubiquitously in human normal tissues, whereas loss of its expression is found in several types of human cancer cell lines (13), and in primary lung cancer (14) and in primary pancreatic cancer (15).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [15]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Probably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductnone givenNegative controls for the specificity of immunohistochemical reactions were performed by replacing the primary antibody with PBS.
“Negative controls for the specificity of immunohistochemical reactions were performed by replacing the primary antibody with PBS.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationPDCD4 exerts its antitumor roles via regulating signal transduction pathways.
“Furthermore, previous studies have shown that PDCD4 exerted its antitumor roles via regulating signal transduction pathways (9,10).”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [9]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [10]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationHuman PDCD4 is highly homologous to mouse PDCD4.
“Human PDCD4 is first cloned from a human glioma library, which is highly homologous to the mouse PDCD4 (11,12).”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [11]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [12]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
The paper relies on this without support.
The three normal glial tissues acquired from tumor adjacent tissue are normal and represent normal glial tissue.
“The three normal glial tissues were all acquired from tumor adjacent tissue.”
The paper relies on this without support.
The 30 glioma samples are representative of human glioma generally.
“In the present study, the expression of PDCD4 in 30 glioma samples was determined at both mRNA and protein levels by means of RT-PCR, Western blotting, and immunohistochemistry.”
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?
miR-21 targets several genes such as PDCD4, TIMP3, and RECK, which are key regulators of apoptotic and metastatic pathways.
“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 [21]
The Introduction describes PDCD4 as a pre-apoptotic tumor suppressor, and the Discussion suggests that its loss in glioma may act through reduced apoptosis. Neither section identifies miR-21 as targeting PDCD4, and our copy does not address TIMP3 or RECK. The central targeting claim is therefore unsupported by this source. (LLM, conf=0.82)
Experimental — accuracy not yet measuredmiR-21 is overexpressed in almost all cancer types, and its upregulation promotes cell proliferation, invasion, and metastatic behavior.
“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 [21]
The Introduction and Discussion report loss of PDCD4 expression in several cancers and in glioma samples; they do not address miR-21. Searches for miR-21 overexpression and for microRNA-related proliferation, invasion, and metastasis found no supporting passage in our copy. Page numbers were not provided. (LLM, conf=0.77)
Experimental — accuracy not yet measuredOverexpressed miR-21 in cell lines can increase the proliferation rate and malignant behavior of the cells.
“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 [21]
The Introduction and Discussion discuss PDCD4 as a tumor suppressor and report its frequent loss of expression in gliomas. A search for miR-21, its overexpression, and effects on cell-line proliferation or malignant behavior found no passage addressing the attributed claim. (LLM, conf=0.76)
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Protein-expression groups account for only 29 of 30 gliomas
MinorIf 23 of the 30 gliomas had no relevant PDCD4 bands, 7 remained, not 6. The stated groups leave one glioma unaccounted for.
Reported 6 · recomputed 7
“In 30 cases of the gliomas, 23 (77%) exhibited no relevant PDCD4 bands and the other 6 showed weak PDCD4 bands, compared with normal brain tissues adjacent to tumor, which showed strong PDCD4 expression (Fig. 2).”
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The Immunology and Biology of Brain Tumors
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- Authors
- Gao, F., Zhang, P., Zhou, C., Li, J., Wang, Q., Zhu, F., Ma, C., Sun, W., & Zhang, L.
- Affiliations
- Shandong University (CN)
- Institute of Immunology (HR)
- Shandong Provincial Hospital (CN)
- Corresponding author
- Zhang, Pin
- Zhang, Lining
- Venue
- Oncology Reports
- Publisher
- Spandidos Publications
- Published
- 2007-01-01
- Volume
- 17
- Issue
- 1
- Pages
- 123-8
- ISSN
- 1021-335X (ISSN-L)
- 1791-2431
- OpenAlex
- W2070433128
- Semantic Scholar
- 26a9de33b9bb133a7e057125005adef5d12159c3
- Cited by
- 100
- References
- 20
- Citations by year
- 2024: 3 · 2023: 1 · 2022: 2 · 2021: 4 · 2020: 4 · 2019: 7 · 2018: 5 · 2017: 2 · 2016: 7 · 2015: 4 · 2014: 5 · 2013: 8 · 2012: 9
- FWCI
- 3.67
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Oncology Reports (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Pennsylvania
- National Natural Science Foundation of China
- National Institutes of Health
- National Key Research and Development Program of China (2006CB503803)
- Topics
- Health Sciences › Medicine › Genetics › Glioma Diagnosis and Treatment
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
- Keywords
- PDCD4, glioma, tumor suppressor, carcinogenesis
- MeSH terms
- Adult, Cell Transformation, Neoplastic, Glioma, Humans, Immunohistochemistry, Middle Aged, RNA, Messenger, Blotting, Western, RNA-Binding Proteins, Reverse Transcriptase Polymerase Chain Reaction, Apoptosis Regulatory Proteins
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