ArticleCancer research2016
G0S2 Suppresses Oncogenic Transformation by Repressing a MYC-Regulated Transcriptional Program.
Article in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 50 citations in OpenAlex.
- Novel Insights into G0S2 as a Central Regulator of Lipid Metabolism and Its Implications for Meat Quality.Animals : an open access journal from MDPI · 2026Review
- Development and validation of mitochondrial metabolism-related genes in the prognostic and immunological characterization of clear cell renal cell carcinoma.Clinical and experimental medicine · 2025Article
- Recent advances on the role of G0S2.Discover oncology · 2025Review
- G0S2: a potential target for NSCLC identified through prognostic models from multi-Omic analysis of regulatory T cell metabolic genes.NPJ precision oncology · 2025Article
- Circulating immune cells exhibit distinct traits linked to metastatic burden in breast cancer.Breast cancer research : BCR · 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
- HSF1 is required for cellular adaptation to daily temperature fluctuations.Scientific reports · 2024Article
- The whole transcriptome analysis using FFPE and fresh tissue samples identifies the molecular fingerprint of osteosarcoma.Experimental biology and medicine (Maywood, N.J.) · 2024Article
- A neutrophil extracellular traps-related classification predicts prognosis and response to immunotherapy in colon cancer.Scientific reports · 2023Article
- The acquisition order of leukemic drug resistance mutations is directed by the selective fitness associated with each resistance mechanism.Scientific reports · 2023Article
- G0S2 promotes antiestrogenic and pro-migratory responses in ER+ and ER- breast cancer cells.Translational oncology · 2023Article
- Article
- A Knowledge-Based Discovery Approach Couples Artificial Neural Networks With Weight Engineering to Uncover Immune-Related Processes Underpinning Clinical Traits of Breast Cancer.Frontiers in immunology · 2022Article
- Appropriate level of cuproptosis may be involved in alleviating pulmonary fibrosis.Frontiers in immunology · 2022Article
- Recent Advances on the Role of ATGL in Cancer.Frontiers in oncology · 2022Review
- Elevated ATGL in colon cancer cells and cancer stem cells promotes metabolic and tumorigenic reprogramming reinforced by obesity.Oncogenesis · 2021Article
- The diversity and breadth of cancer cell fatty acid metabolism.Cancer & metabolism · 2021Review
- Adipose triglyceride lipase activity regulates cancer cell proliferation via AMP-kinase and mTOR signaling.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020Article
- CGI-58: Versatile Regulator of Intracellular Lipid Droplet Homeostasis.Advances in experimental medicine and biology · 2020Review
- Characterization of four subtypes in morphologically normal tissue excised proximal and distal to breast cancer.NPJ breast cancer · 2020Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Methylation-mediated silencing of G0-G1 switch gene 2 (G0S2) has been detected in a variety of solid tumors, whereas G0S2 induction is associated with remissions in patients with acute promyelocytic leukemia, implying that G0S2 may possess tumor suppressor activity. In this study, we clearly demonstrate that G0S2 opposes oncogene-induced transformation using G0s2-null immortalized mouse embryonic fibroblasts (MEF). G0s2-null MEFs were readily transformed with HRAS or EGFR treatment compared with wild-type MEFs. Importantly, restoration of G0S2 reversed HRAS-driven transformation. G0S2 is known to regulate fat metabolism by attenuating adipose triglyceride lipase (ATGL), but repression of oncogene-induced transformation by G0S2 was independent of ATGL inhibition. Gene expression analysis revealed an upregulation of gene signatures associated with transformation, proliferation, and MYC targets in G0s2-null MEFs. RNAi-mediated ablation and pharmacologic inhibition of MYC abrogated oncogene-induced transformation of G0s2-null MEFs. Furthermore, we found that G0S2 was highly expressed in normal breast tissues compared with malignant tissue. Intriguingly, high levels of G0S2 were also associated with a decrease in breast cancer recurrence rates, especially in estrogen receptor-positive subtypes, and overexpression of G0S2 repressed the proliferation of breast cancer cells in vitro. Taken together, these findings indicate that G0S2 functions as a tumor suppressor in part by opposing MYC activity, prompting further investigation of the mechanisms by which G0S2 silencing mediates MYC-induced oncogenesis in other malignancies.
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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.