ArticleJournal of neuro-oncology2019
G3BP1 knockdown sensitizes U87 glioblastoma cell line to Bortezomib by inhibiting stress granules assembly and potentializing apoptosis.
Article in Journal of neuro-oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- The Role of Long Noncoding RNAs in Modulation of Stress Granules in Cancer.Journal of cellular and molecular medicine · 2026Review
- Review
- Hypoxia-induced PRMT6 expression promotes temozolomide chemoresistance in glioblastoma via G3BP1.Journal of translational medicine · 2026Article
- Pharmacological modulation of stress granulesFrontiers in pharmacology · 2026Review
- Stress Granules: Novel Regulators of Programmed Cell Death.Mini reviews in medicinal chemistry · 2026Review
- Stress granules promote quiescence by enhancing p21 levels and reducing phospho-Rb.RNA (New York, N.Y.) · 2025Article
- Investigating the Cellular Responses to Combined Nisin and Urolithin B Treatment (7:3) in HKB-11 Lymphoma Cells.International journal of molecular sciences · 2025Article
- Review
- Role(s) of G3BPs in Human Pathogenesis.The Journal of pharmacology and experimental therapeutics · 2023Review
- QKI shuttles internal mCell · 2023Article
- G3BP1 regulates breast cancer cell proliferation and metastasis by modulating PKCζ.Frontiers in genetics · 2022Article
- Stress Granules in the Anti-Cancer Medications Mechanism of Action: A Systematic Scoping Review.Frontiers in oncology · 2021Article
- Inhibition of PLK4 might enhance the anti-tumour effect of bortezomib on glioblastoma via PTEN/PI3K/AKT/mTOR signalling pathway.Journal of cellular and molecular medicine · 2020Article
- RNA Binding Protein Motif 3 Inhibits Oxygen-Glucose Deprivation/Reoxygenation-Induced Apoptosis Through Promoting Stress Granules Formation in PC12 Cells and Rat Primary Cortical Neurons.Frontiers in cellular neuroscience · 2020Article
- Understanding the roles of stress granule during chemotherapy for patients with malignant tumors.American journal of cancer research · 2020Review
- Mechanisms of tRNA-derived fragments and tRNA halves in cancer treatment resistance.Biomarker research · 2020Review
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
introductionGlioblastoma multiforme (GBM) is the most lethal form of gliomas. New therapies are currently in development to tackle treatment limitations such as chemotherapy resistance. One mechanism of resistance may be the stress granules (SG) assembly, a stress-related cellular response that allows cells to recruit and protect mRNAs during stress. SG are composed of various proteins, being G3BP1 a core element that enucleates and results in SG assembly. Here, we aimed to evaluate the effects of inhibiting the G3PB1 expression in the chemotherapeutical-induced cell death of the U87 glioblastoma cell line. MATERIALS AND
methodsG3BP1 mRNA and protein expression were modulated with short-interference RNA (siRNA). The viability of U87 cells after Bortezomib (BZM), a proteasome inhibitor, and Temozolomide (TMZ), an alkylating agent, was assessed by MTT assay. Apoptosis was evaluated by staining cells with Annexin-V/7-AAD and analyzing by flow cytometry. Caspase-3 activation was evaluated by immunoblotting. The chorioallantoic membrane in vivo assay was used to evaluate angiogenesis.
resultsWhen G3BP1 was knocked-down, the SG assembly was reduced and the BZM-treated cells, but not TMZ-treated cells, had a significant increase in the apoptotic response. Corroborating this data, we observed increased Caspase-3 activation in the BZM-treated and G3BP1-knocked-down cells when compared to vehicle-treated and scramble-transfected cells. Worth mentioning, the conditioned culture medium of G3BP1-knocked-down BZM-treated cells inhibited angiogenesis when compared to controls.
conclusionOur data suggest G3BP1 knockdown diminishes SG formation and stimulates BZM-induced apoptosis of U87 cells in vitro, in addition to inhibiting glioblastoma-induced angiogenesis in vivo.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.