ArticleOncotarget2015
Inhibition of adipose triglyceride lipase (ATGL) by the putative tumor suppressor G0S2 or a small molecule inhibitor attenuates the growth of cancer cells.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 88 citations in OpenAlex.
- Lipid metabolism in colorectal cancer: dual roles and statin therapy.Discover oncology · 2025Review
- 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
- Adipose Triglyceride Lipase Is a Therapeutic Target in Advanced Prostate Cancer That Promotes Metabolic Plasticity.Cancer research · 2024Article
- New Insights into the Link Between Melanoma and Obesity.Advances in experimental medicine and biology · 2024Review
- CD4+ T cells regulate sickness-induced anorexia and fat wasting during a chronic parasitic infection.Cell reports · 2023Article
- G0S2 promotes antiestrogenic and pro-migratory responses in ER+ and ER- breast cancer cells.Translational oncology · 2023Article
- BETi enhance ATGL expression and its lipase activity to exert their antitumoral effects in triple-negative breast cancer (TNBC) cells.Journal of experimental & clinical cancer research : CR · 2023Article
- Loss of G0/G1 switch gene 2 (G0S2) promotes disease progression and drug resistance in chronic myeloid leukaemia (CML) by disrupting glycerophospholipid metabolism.Clinical and translational medicine · 2022Article
- Approaches to Measuring the Activity of Major Lipolytic and Lipogenic Enzymes In Vitro and Ex Vivo.International journal of molecular sciences · 2022Review
- Mitotane Targets Lipid Droplets to Induce Lipolysis in Adrenocortical Carcinoma.Endocrinology · 2022Article
- Small-Molecule Inhibitors Targeting Lipolysis in Human Adipocytes.Journal of the American Chemical Society · 2022Article
- Lipid Droplets in Cancer: From Composition and Role to Imaging and Therapeutics.Molecules (Basel, Switzerland) · 2022Review
- Recent Advances on the Role of ATGL in Cancer.Frontiers in oncology · 2022Review
- Adding fuel to the fire: The lipid droplet and its associated proteins in cancer progression.International journal of biological sciences · 2022Review
- Elevated ATGL in colon cancer cells and cancer stem cells promotes metabolic and tumorigenic reprogramming reinforced by obesity.Oncogenesis · 2021Article
- Review
- Article
- Motility Plays an Important Role in the Lifetime of Mammalian Lipid Droplets.International journal of molecular sciences · 2021Review
- Adipose triglyceride lipase promotes the proliferation of colorectal cancer cells via enhancing the lipolytic pathway.Journal of cellular and molecular medicine · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The G0/G1 switch gene 2 (G0S2) is methylated and silenced in a wide range of human cancers. The protein encoded by G0S2 is an endogenous inhibitor of lipid catabolism that directly binds adipose triglyceride lipase (ATGL). ATGL is the rate-limiting step in triglyceride metabolism. Although the G0S2 gene is silenced in cancer, the impact of ATGL in the growth and survival of cancer cells has never been addressed. Here we show that ectopic expression of G0S2 in non-small cell lung carcinomas (NSCL) inhibits triglyceride catabolism and results in lower cell growth. Similarly, knockdown of ATGL increased triglyceride levels, attenuated cell growth and promoted apoptosis. Conversely, knockdown of endogenous G0S2 enhanced the growth and invasiveness of cancer cells. G0S2 is strongly induced in acute promyelocytic leukemia (APL) cells in response to all trans retinoic acid (ATRA) and we show that inhibition of ATGL in these cells by G0S2 is required for efficacy of ATRA treatment. Our data uncover a novel tumor suppressor mechanism by which G0S2 directly inhibits activity of a key intracellular lipase. Our results suggest that elevated ATGL activity may be a general property of many cancer types and potentially represents a novel target for chemotherapy.
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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.