ArticleCell death & disease2019
mTOR direct crosstalk with STAT5 promotes de novo lipid synthesis and induces hepatocellular carcinoma.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 57 citations in OpenAlex.
- Genetic deletion of miR-200a/200b increases growth and feed conversion efficiency in yellow catfish.Science China. Life sciences · 2026Article
- HIF-2α induction in de novo lipogenesis in metabolic dysfunction-associated steatohepatitis is dependent on IL-21 signaling.The Journal of biological chemistry · 2026Article
- Perilipin1 mediates milk fat synthesis in bovine mammary epithelial cells through SREBP1 phosphorylation.Animal biotechnology · 2025Article
- Article
- A feedforward loop between STAT1 and YAP1 stimulates lipid biosynthesis, accelerates tumor growth, and promotes chemotherapy resistance in mutant KRAS colorectal cancer.Communications biology · 2025Article
- CXCL6 Reshapes Lipid Metabolism and Induces Neutrophil Extracellular Trap Formation in Cholangiocarcinoma Progression and Immunotherapy Resistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Multiomics identifies tumor-intrinsic SREBP1 driving immune exclusion in hepatocellular carcinoma.Journal for immunotherapy of cancer · 2025Article
- The immune mechanism of the mTOR/ACC1/CPT1A fatty acid oxidation signaling pathway in Hashimoto's thyroiditis.Journal of endocrinological investigation · 2025Article
- Metabolic reprogramming in hepatocellular carcinoma: mechanisms and therapeutic implications.Experimental & molecular medicine · 2025Review
- DLAT is involved in ovarian cancer progression by modulating lipid metabolism through the JAK2/STAT5A/SREBP1 signaling pathway.Cancer cell international · 2025Article
- Identifying the Crucial Biomarker of MASH-Related HCC.Combinatorial chemistry & high throughput screening · 2025Article
- STAT5: Understanding the Biology of KRASJournal of cellular and molecular medicine · 2024Article
- PAX6 promotes neuroendocrine phenotypes of prostate cancer via enhancing MET/STAT5A-mediated chromatin accessibility.Journal of experimental & clinical cancer research : CR · 2024Article
- The Potential Role of C-Reactive Protein in Metabolic-Dysfunction-Associated Fatty Liver Disease and Aging.Biomedicines · 2023Review
- The Role of mTOR Inhibitors after Liver Transplantation for Hepatocellular Carcinoma.Current oncology (Toronto, Ont.) · 2023Review
- STAT proteins in cancer: orchestration of metabolism.Nature reviews. Cancer · 2023Review
- ARID2 mitigates hepatic steatosis via promoting the ubiquitination of JAK2.Cell death and differentiation · 2023Article
- mTOR: A Potential New Target in Nonalcoholic Fatty Liver Disease.International journal of molecular sciences · 2022Review
- NUMB facilitates autophagy initiation through targeting SCFCell death and differentiation · 2022Article
- Lipid metabolism, inflammation, and foam cell formation in health and metabolic disorders: targeting mTORC1.Journal of molecular medicine (Berlin, Germany) · 2021Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) can be the last step of nonalcoholic fatty liver disease (NAFLD) evolution, and the main characteristic of NAFLD is alteration in lipid metabolism. However, the mechanisms of abnormal lipid metabolism in NAFLD and HCC progression are yet to be identified. Here, we demonstrate that liver-specific activation of mTORC1 promoted the expression of lipid synthesis genes and lead to the development of spontaneous HCC. Genetic mouse models developed spontaneous HCC along with increased expressions of SREBP1, ACC1 and FASN. In addition, high levels of p-STAT5 were observed in the livers and particularly evident in the tumor area. And the synthesis of p-STAT5 was increased in patients along with the increase in SREBP1 synthesis in clinical samples. Moreover, mTORC1 interacts with and phosphorylates the STAT5 in hepatocytes. In conclusion, our data suggested that mTORC1 upregulates SREBP1 transcription via crosstalk with the STAT5 pathway which contributes to the NAFLD-related HCC pathogenesis. And the inhibitor of SREBP1 and mTOR may help to prevent HCC in clinical NAFLD patients.
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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.