{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tang W"],"funding":["Research Grants Council, University Grants Committee","Terry Fox Foundation","Li Ka Shing Foundation","AstraZeneca"],"pagination":["834-847"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9243114"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["19(7)"],"pubmed_abstract":["Obesity is a major risk factor for cancers including hepatocellular carcinoma (HCC) that develops from a background of non-alcoholic fatty liver disease (NAFLD). Hypercholesterolemia is a common comorbidity of obesity. Although cholesterol biosynthesis mainly occurs in the liver, its role in HCC development of obese people remains obscure. Using high-fat high-carbohydrate diet-associated orthotopic and spontaneous NAFLD-HCC mouse models, we found that hepatic cholesterol accumulation in obesity selectively suppressed natural killer T (NKT) cell-mediated antitumor immunosurveillance. Transcriptome analysis of human liver revealed aberrant cholesterol metabolism and NKT cell dysfunction in NAFLD patients. Notably, cholesterol-lowering rosuvastatin restored NKT expansion and cytotoxicity to p"],"journal":["Cellular & molecular immunology"],"pubmed_title":["Aberrant cholesterol metabolic signaling impairs antitumor immunosurveillance through natural killer T cell dysfunction in obese liver."],"pmcid":["PMC9243114"],"funding_grant_id":["14105419","14104820","Terry Fox Foundation","Li Ka Shing Foundation","C4045-18W","AstraZeneca Research Program (2017)"],"pubmed_authors":["Lai PBS","Liang Z","Mok MTS","Ng KKC","Wong VWS","Zhang L","Wong SKH","Wang J","Hou Y","Wu H","Liu X","Xiong Z","To KF","Yeung PC","Lee HM","Kong APS","Cheng ASL","Tang W","Sun H","Wong J","Sung JJY","Zhou J","Li J","Feng Y","Zeng X","Lam CCH","Yang W","Tian X","Lu J","Leung HHW","Chan AWH"],"additional_accession":[]},"is_claimable":false,"name":"Aberrant cholesterol metabolic signaling impairs antitumor immunosurveillance through natural killer T cell dysfunction in obese liver.","description":"Obesity is a major risk factor for cancers including hepatocellular carcinoma (HCC) that develops from a background of non-alcoholic fatty liver disease (NAFLD). Hypercholesterolemia is a common comorbidity of obesity. Although cholesterol biosynthesis mainly occurs in the liver, its role in HCC development of obese people remains obscure. Using high-fat high-carbohydrate diet-associated orthotopic and spontaneous NAFLD-HCC mouse models, we found that hepatic cholesterol accumulation in obesity selectively suppressed natural killer T (NKT) cell-mediated antitumor immunosurveillance. Transcriptome analysis of human liver revealed aberrant cholesterol metabolism and NKT cell dysfunction in NAFLD patients. Notably, cholesterol-lowering rosuvastatin restored NKT expansion and cytotoxicity to p","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jul","modification":"2026-05-28T01:31:53.198Z","creation":"2025-02-19T01:18:13.107Z"},"accession":"S-EPMC9243114","cross_references":{"pubmed":["35595819"],"doi":["10.1038/s41423-022-00872-3"]}}