Downregulation of SNRPG induces cell cycle arrest and sensitizes human glioblastoma cells to temozolomide by targeting Myc through a p53-dependent signaling pathway
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Objective: Temozolomide (TMZ) is commonly used for glioblastoma multiforme (GBM) chemotherapy. However, drug resistance limits its therapeutic effect in GBM treatment. RNA-binding proteins (RBPs) have vital roles in posttranscriptional events. While disturbance of RBP-RNA network activity is potentially associated with cancer development, the precise mechanisms are not fully known. The SNRPG gene, encoding small nuclear ribonucleoprotein polypeptide G, was recently found to be related to cancer incidence, but its exact function has yet to be elucidated. Methods: SNRPG knockdown was achieved via short hairpin RNAs. Gene expression profiling and Western blot analyses were used to identify potential glioma cell growth signaling pathways affected by SNRPG. Xenograft tumors were examined to determine the carcinogenic effects of SNRPG on glioma tissues. Results: The SNRPG-mediated inhibitory effect on glioma cells might be due to the targeted prevention of Myc and p53. In addition, the effects of SNRPG loss on p53 levels and cell cycle progression were found to be Myc-dependent. Furthermore, SNRPG was increased in TMZ-resistant GBM cells, and downregulation of SNRPG potentially sensitized resistant cells to TMZ, suggesting that SNRPG deficiency decreases the chemoresistance of GBM cells to TMZ via the p53 signaling pathway. Our data confirmed that SNRPG suppression sensitizes GBM cells to TMZ by targeting Myc via the p53 signaling cascade. Conclusions: These results indicated that SNRPG is a probable molecular target of GBM and suggested that suppressing SNRPG in resistant GBM cells might be a substantially beneficial method for overcoming essential drug resistance.
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The clinical efficacy of MDM2 inhibitors may mainly rely on reversible cell cycle arrest rather than direct induction of cell death through p53-dependent signaling pathway.
“Therefore, the clinical efficacy of MDM2 inhibitors may mainly rely on the reversible cell cycle arrest rather than direct induction of cell death through p53-dependent signaling pathway [89–91].”
From Targeting p53–MDM2 interaction by small-molecule inhibitors: learning from MDM2 inhibitors in clinical trials (2022) · cites this paper as [90]
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Effects of APT20TTMG, a modulator of the U1 snRNP complex, in glioblastoma models
Leal, C. B. Q. D. S., Moreira, C. G., Sinatti, V. V. C., Soares, E. S., Rafii, M. S., & Bottos, R. M. (2025) · Medical Oncology · doi:10.1007/s12032-025-03057-w
- Authors
- Lan, Y., Lou, J., Hu, J., Yu, Z., Lyu, W., & Zhang, B.
- Affiliations
- Dalian Medical University (CN)
- Jinan University (CN)
- Corresponding author
- Lyu, Wen
- Zhang, Bo
- Venue
- Cancer Biology and Medicine
- Publisher
- China Anti-cancer Association
- Published
- 2020
- Volume
- 17
- Issue
- 1
- Pages
- 112-131
- ISSN
- 2095-3941 (ISSN-L)
- PMC
- PMC7142844
- OpenAlex
- W3019450950
- Cited by
- 46
- References
- 51
- Citations by year
- 2026: 1 · 2025: 7 · 2024: 5 · 2023: 9 · 2022: 14 · 2021: 8 · 2020: 2
- FWCI
- 4.27
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Cancer Biology and Medicine (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Health Sciences › Medicine › Genetics › Glioma Diagnosis and Treatment
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Research and Splicing
- Keywords
- glioblastoma, temozolomide, drug resistance, c-Myc, p53 pathway, cell cycle arrest, RNA-binding proteins, chemosensitization, post-transcriptional regulation
- MeSH terms
- Temozolomide, Adult, Aged, Animals, Brain, Brain Neoplasms, Female, Glioblastoma, Humans, Male, Middle Aged, Signal Transduction, Down-Regulation, Gene Expression Regulation, Neoplastic, Tumor Suppressor Protein p53, Proto-Oncogene Proteins c-myc, Drug Resistance, Neoplasm, Xenograft Model Antitumor Assays, Cell Line, Tumor, Mice, snRNP Core Proteins, Gene Knockdown Techniques
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.
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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