{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Fu R"],"funding":["China Postdoctoral Science Foundation","Natural Science Foundation of Tianjin Municipal Science and Technology Commission (Natural Science Foundation of Tianjin Municipal Science & Technology Commission)","National Natural Science Foundation of China (National Science Foundation of China)"],"pagination":["325"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11082151"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(5)"],"pubmed_abstract":["Cholesterol metabolism reprogramming is one of the significant characteristics of hepatocellular carcinoma (HCC). Cholesterol increases the risk of epithelial-mesenchymal transition (EMT) in cancer. Sterol O-acyltransferases 1 (SOAT1) maintains the cholesterol homeostasis. However, the exact mechanistic contribution of SOAT1 to EMT in HCC remains unclear. Here we demonstrated that SOAT1 positively related to poor prognosis of HCC, EMT markers and promoted cell migration and invasion in vitro, which was mediated by the increased cholesterol in plasmalemma and cholesterol esters accumulation. Furthermore, we reported that SOAT1 disrupted cholesterol metabolism homeostasis to accelerate tumorigenesis and development in HCC xenograft and NAFLD-HCC. Also, we detected that nootkatone, a sesquite"],"journal":["Cell death & disease"],"pubmed_title":["SOAT1 regulates cholesterol metabolism to induce EMT in hepatocellular carcinoma."],"pmcid":["PMC11082151"],"funding_grant_id":["23JCYBJC00850","2022M712374","81902441","82072709"],"pubmed_authors":["Fu R","Xue W","Li X","Zheng J","Liang J","Zhang M","Meng J","Wang L"],"additional_accession":[]},"is_claimable":false,"name":"SOAT1 regulates cholesterol metabolism to induce EMT in hepatocellular carcinoma.","description":"Cholesterol metabolism reprogramming is one of the significant characteristics of hepatocellular carcinoma (HCC). Cholesterol increases the risk of epithelial-mesenchymal transition (EMT) in cancer. Sterol O-acyltransferases 1 (SOAT1) maintains the cholesterol homeostasis. However, the exact mechanistic contribution of SOAT1 to EMT in HCC remains unclear. Here we demonstrated that SOAT1 positively related to poor prognosis of HCC, EMT markers and promoted cell migration and invasion in vitro, which was mediated by the increased cholesterol in plasmalemma and cholesterol esters accumulation. Furthermore, we reported that SOAT1 disrupted cholesterol metabolism homeostasis to accelerate tumorigenesis and development in HCC xenograft and NAFLD-HCC. Also, we detected that nootkatone, a sesquite","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 May","modification":"2026-07-15T09:31:01.634Z","creation":"2026-07-02T03:12:38.313Z"},"accession":"S-EPMC11082151","cross_references":{"pubmed":["38724499"],"doi":["10.1038/s41419-024-06711-9"]}}