ArticleCell metabolism2014
Liver damage, inflammation, and enhanced tumorigenesis after persistent mTORC1 inhibition.
Article in Cell metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 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
109 citing papers in PubMed, 176 citations in OpenAlex.
- mTORC1-TFEB/TFE3 signaling is associated with bile acid diversification during hepatic metabolic adaptation.Science advances · 2026Article
- Molecular mechanisms and pathogenesis of MASH.Nature · 2026Review
- Loss of hepatocyte PI3Kα reduces hepatocellular carcinoma and hepatocyte proliferation in association with altered lipid metabolism.JHEP reports : innovation in hepatology · 2026Article
- Metabolic dysfunction-associated steatotic liver disease and steatohepatitis-associated hepatocarcinoma preclinical models.Nature reviews. Gastroenterology & hepatology · 2026Review
- p53 regulates glucose metabolic reprogramming in MASLD-related hepatocellular carcinoma via modulating mitochondrial pyruvate carriers.Hepatology international · 2026Article
- Role of cellular senescence in hepatic diseases (Review).International journal of molecular medicine · 2025Review
- Folliculin depletion results in liver cell damage and cholangiocarcinoma through MiT/TFE activation.Cell death and differentiation · 2025Article
- Article
- S-adenosylmethionine deficit disrupts very low-density lipoprotein metabolism promoting liver lipid accumulation in mice.Journal of lipid research · 2025Article
- RAP1A suppresses hepatic steatosis by regulating amino acid-mediated mTORC1 activation.JHEP reports : innovation in hepatology · 2025Article
- Hepatocellular carcinoma: signaling pathways and therapeutic advances.Signal transduction and targeted therapy · 2025Review
- Unveiling the cancer risk nexus of the steatotic liver.Trends in endocrinology and metabolism: TEM · 2024Review
- MHY1485 promotes adriamycin sensitivity in HepG2 cells by inhibiting autophagy.Functional & integrative genomics · 2024Article
- RBM45 reprograms lipid metabolism promoting hepatocellular carcinoma via Rictor and ACSL1/ACSL4.Oncogene · 2024Article
- Immunotherapy in liver cancer: overcoming the tolerogenic liver microenvironment.Frontiers in immunology · 2024Review
- Hepatocellular loss of mTOR aggravates tumor burden in nonalcoholic steatohepatitis-related HCC.Neoplasia (New York, N.Y.) · 2023Article
- mTOR-dependent loss of PON1 secretion and antiphospholipid autoantibody production underlie autoimmunity-mediated cirrhosis in transaldolase deficiency.Journal of autoimmunity · 2023Article
- Regulation of mTOR Signaling: Emerging Role of Cyclic Nucleotide-Dependent Protein Kinases and Implications for Cardiometabolic Disease.International journal of molecular sciences · 2023Review
- MPEP Attenuates Intrahepatic Fat Accumulation in Obese Mice.International journal of molecular sciences · 2023Article
- Combining Metformin and Drug-Loaded Kidney-Targeting Micelles for Polycystic Kidney Disease.Cellular and molecular bioengineering · 2023Article
49 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
Abstract
Obesity can result in insulin resistance, hepatosteatosis, and nonalcoholic steatohepatitis (NASH) and increases liver cancer risk. Obesity-induced insulin resistance depends, in part, on chronic activation of mammalian target of rapamycin complex 1 (mTORC1), which also occurs in human and mouse hepatocellular carcinoma (HCC), a frequently fatal liver cancer. Correspondingly, mTORC1 inhibitors have been considered as potential NASH and HCC treatments. Using a mouse model in which high-fat diet enhances HCC induction by the hepatic carcinogen DEN, we examined whether mTORC1 inhibition attenuates liver inflammation and tumorigenesis. Notably, rapamycin treatment or hepatocyte-specific ablation of the specific mTORC1 subunit Raptor resulted in elevated interleukin-6 (IL-6) production, activation of signal transducer and activator of transcription 3 (STAT3), and enhanced HCC development, despite a transient reduction in hepatosteatosis. These results suggest that long-term rapamycin treatment, which also increases IL-6 production in humans, is unsuitable for prevention or treatment of obesity-promoted liver cancer.
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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.