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- W2897934013 abstract "Abstract The underlining mechanisms of dietary cholesterol and nonalcoholic steatohepatitis (NASH) in contributing to hepatocellular carcinoma (HCC) remain undefined. Here we demonstrated that high-fat-non-cholesterol-fed mice developed simple steatosis, whilst high-fat-high-cholesterol-fed mice developed NASH. Moreover, dietary cholesterol induced larger and more numerous NASH-HCCs than non-cholesterol-induced steatosis-HCCs in diethylnitrosamine-treated mice. NASH-HCCs displayed significantly more aberrant gene expression-enriched signaling pathways and more non-synonymous somatic mutations than steatosis-HCCs (335 ± 84/sample vs 43 ± 13/sample). Integrated genetic and expressional alterations in NASH-HCCs affected distinct genes pertinent to five pathways: calcium, insulin, cell adhesion, axon guidance and metabolism. Some of the novel aberrant gene expression, mutations and core oncogenic pathways identified in cholesterol-associated NASH-HCCs in mice were confirmed in human NASH-HCCs, which included metabolism-related genes ( ALDH18A1, CAD , CHKA , POLD4 , PSPH and SQLE ) and recurrently mutated genes ( RYR1 , MTOR , SDK1 , CACNA1H and RYR2) . These findings add insights into the link of cholesterol to NASH and NASH-HCC and provide potential therapeutic targets." @default.
- W2897934013 created "2018-10-26" @default.
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- W2897934013 date "2018-10-26" @default.
- W2897934013 modified "2023-10-16" @default.
- W2897934013 title "Dietary cholesterol promotes steatohepatitis related hepatocellular carcinoma through dysregulated metabolism and calcium signaling" @default.
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- W2897934013 doi "https://doi.org/10.1038/s41467-018-06931-6" @default.
- W2897934013 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6203711" @default.
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- W2897934013 hasPublicationYear "2018" @default.
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