ArticleJournal of experimental & clinical cancer research : CR2019
Lipolytic inhibitor G0S2 modulates glioma stem-like cell radiation response.
Article in Journal of experimental & clinical cancer research : CR, 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 23 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- Molecular insights into DNA damage response plasticity in glioma stem cells.Communications biology · 2026Review
- Identification of an age-related monocyte-derived macrophages characteristic genes-based signature for high-grade diffuse glioma.Scientific reports · 2026Article
- Clinical significance and oncogenic role of ECHDC2 in glioblastoma: a comprehensive analysis based on bioinformatics andFrontiers in genetics · 2026Article
- Molecular characterization of macrophage-related prognostic factors in glioblastoma revealed by combined analysis on single-cell and bulk transcriptome data.Discover oncology · 2025Article
- EGFR and EGFRvIII coopt host defense pathways promoting progression in glioblastoma.Neuro-oncology · 2025Article
- Mutation on JmjC domain of UTX impaired its antitumor effects in pancreatic cancer via inhibiting G0S2 expression and activating the Toll-like signaling pathway.Molecular medicine (Cambridge, Mass.) · 2024Article
- Exosomal circZNF800 Derived from Glioma Stem-like Cells Regulates Glioblastoma Tumorigenicity via the PIEZO1/Akt Axis.Molecular neurobiology · 2024Article
- Exploring the prognostic value and biological pathways of transcriptomics and radiomics patterns in glioblastoma multiforme.Heliyon · 2024Article
- Exploring MiR-484 Regulation byBiomedicines · 2024Article
- Identification of Necroptosis-related Molecular Subtypes and Construction of Necroptosis-related Gene Signature for Glioblastoma Multiforme.Current medicinal chemistry · 2024Article
- The Mechanism of Ubiquitination or Deubiquitination Modifications in Regulating Solid Tumor Radiosensitivity.Biomedicines · 2023Review
- IDH1Scientific reports · 2023Article
- G0S2 promotes antiestrogenic and pro-migratory responses in ER+ and ER- breast cancer cells.Translational oncology · 2023Article
- Targeting copper death genotyping associated gene RARRES2 suppresses glioblastoma progression and macrophages infiltration.Cancer cell international · 2023Article
- Emerging Roles of RNF168 in Tumor Progression.Molecules (Basel, Switzerland) · 2023Review
- Multifaceted regulation and functions of 53BP1 in NHEJ‑mediated DSB repair (Review).International journal of molecular medicine · 2022Review
- Gpx3 and Egr1 Are Involved in Regulating the Differentiation Fate of Cardiac Fibroblasts under Pressure Overload.Oxidative medicine and cellular longevity · 2022Article
- The role of E3 ubiquitin ligases in the development and progression of glioblastoma.Cell death and differentiation · 2021Review
- Article
- Biological Adaptations of Tumor Cells to Radiation Therapy.Frontiers in oncology · 2021Review
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundIonizing radiation (IR) therapy is the standard first-line treatment for newly diagnosed patients with glioblastoma (GBM), the most common and malignant primary brain tumor. However, the effects of IR are limited due to the aberrant radioresistance of GBM.
methodsTranscriptome analysis was performed using RNA-seq in radioresistant patient-derived glioma stem-like cells (GSCs). Survival of glioma patient and mice bearing-brain tumors was analyzed by Kaplan-Meier survival analysis. Lipid droplet and γ-H2AX foci-positive cells were evaluated using immunofluorescence staining.
resultsLipolytic inhibitor G0/G1 switch gene 2 (G0S2) is upregulated in radioresistant GSCs and elevated in clinical GBM. GBM patients with high G0S2 expression had significantly shorter overall survival compared with those with low expression of G0S2. Using genetic approaches targeting G0S2 in glioma cells and GSCs, we found that knockdown of G0S2 promoted lipid droplet turnover, inhibited GSC radioresistance, and extended survival of xenograft tumor mice with or without IR. In contrast, overexpression of G0S2 promoted glioma cell radiation resistance. Mechanistically, high expression of G0S2 reduced lipid droplet turnover and thereby attenuated E3 ligase RNF168-mediated 53BP1 ubiquitination through activated the mechanistic target of rapamycin (mTOR)-ribosomal S6 kinase (S6K) signaling and increased 53BP1 protein stability in response to IR, leading to enhanced DNA repair and glioma radioresistance.
conclusionsOur findings uncover a new function for lipolytic inhibitor G0S2 as an important regulator for GSC radioresistance, suggesting G0S2 as a potential therapeutic target for treating gliomas.
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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.