ArticleOncogene2019
Forcing ATGL expression in hepatocarcinoma cells imposes glycolytic rewiring through PPAR-α/p300-mediated acetylation of p53.
Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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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
30 citing papers in PubMed, 53 citations in OpenAlex.
- ATGL sensitizes hepatocellular carcinoma cells to genotoxic drugs by modulating p53 acetylation/phosphorylation status.Cell death discovery · 2026Article
- The impact of epigenetics on tumor metabolism: Friend or foe in drug response?Frontiers in epigenetics and epigenomics · 2026Review
- Rethinking carnitine palmitoyltransferase II and liver stem cells in metabolic dysfunction-associated fatty liver disease-related hepatocellular carcinoma.World journal of gastroenterology · 2025Article
- Hypoxia-Induced Reactive Oxygen Species: Their Role in Cancer Resistance and Emerging Therapies to Overcome It.Antioxidants (Basel, Switzerland) · 2025Review
- Adipose Triglyceride Lipase Is a Therapeutic Target in Advanced Prostate Cancer That Promotes Metabolic Plasticity.Cancer research · 2024Article
- [Research progress of long-chain non-coding RNA in lipid metabolism reprogramming in primary hepatocellular carcinoma].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2024Article
- Exploring the impact of lipid droplets on the evolution and progress of hepatocarcinoma.Frontiers in cell and developmental biology · 2024Review
- Microfibrillar-associated protein 5 suppresses adipogenesis by inhibiting essential coactivator of PPARγ.Scientific reports · 2023Article
- Ambra1 modulates the tumor immune microenvironment and response to PD-1 blockade in melanoma.Journal for immunotherapy of cancer · 2023Article
- Review
- Small-Molecule Inhibitors Targeting Lipolysis in Human Adipocytes.Journal of the American Chemical Society · 2022Article
- 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
- Roles and regulation of histone acetylation in hepatocellular carcinoma.Frontiers in genetics · 2022Review
- Adipose Triglyceride Lipase in Hepatic Physiology and Pathophysiology.Biomolecules · 2021Review
- Review
- Adipose triglyceride lipase promotes the proliferation of colorectal cancer cells via enhancing the lipolytic pathway.Journal of cellular and molecular medicine · 2021Article
- ROS-dependent HIF1α activation under forced lipid catabolism entails glycolysis and mitophagy as mediators of higher proliferation rate in cervical cancer cells.Journal of experimental & clinical cancer research : CR · 2021Article
- Review
- Downregulation of adipose triglyceride lipase by EB viral-encoded LMP2A links lipid accumulation to increased migration in nasopharyngeal carcinoma.Molecular oncology · 2020Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Metabolic reprogramming is a typical feature of cancer cells aimed at sustaining high-energetic demand and proliferation rate. Here, we report clear-cut evidence for decreased expression of the adipose triglyceride lipase (ATGL), the first and rate-limiting enzyme of triglyceride hydrolysis, in both human and mouse-induced hepatocellular carcinoma (HCC). We identified metabolic rewiring as major outcome of ATGL overexpression in HCC-derived cell lines. Indeed, ATGL slackened both glucose uptake/utilization and cell proliferation in parallel with increased oxidative metabolism of fatty acids and enhanced mitochondria capacity. We ascribed these ATGL-downstream events to the activity of the tumor-suppressor p53, whose protein levels-but not transcript-were upregulated upon ATGL overexpression. The role of p53 was further assessed by abrogation of the ATGL-mediated effects upon p53 silencing or in p53-null hepatocarcinoma Hep3B cells. Furthermore, we provided insights on the molecular mechanisms governed by ATGL in HCC cells, identifying a new PPAR-α/p300 axis responsible for p53 acetylation/accumulation. Finally, we highlighted that ATGL levels confer different susceptibility of HCC cells to common therapeutic drugs, with ATGL overexpressing cells being more resistant to glycolysis inhibitors (e.g., 2-deoxyglucose and 3-bromopyruvate), compared to genotoxic compounds. Collectively, our data provide evidence for a previously uncovered tumor-suppressor function of ATGL in HCC, with the outlined molecular mechanisms shedding light on new potential targets for anticancer therapy.
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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.