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• W3012226795 endingPage "109055" @default.
• W3012226795 startingPage "109055" @default.
• W3012226795 abstract "Alcoholism synergizes the development of the hepatocellular carcinoma (HCC) in patients infected with hepatitis B or C virus (HBV or HCV). Tumor-initiating stem-like cells (TICs) are refractory to therapy and have expression of stemness transcription factors. Leaky-gut-derived endotoxin stimulates TLR4-NANOG pathway that skews asymmetric cell division and that metabolically reprograms hepatocytes/liver progenitor cells, leading to self-renewal. TICs isolated from mouse HCC models or human HCCs are tumorigenic and have p53 degradation via phosphorylation of the protective protein NUMB and its dissociation from p53 by the oncofetal protein TBC1D15. Furthermore, dysregulation of lncRNA promotes genesis of TICs, leading to HCC development. This review describes roles of cell fate decision, metabolic reprogramming and lncRNA for TIC genesis and liver oncogenesis. This project was supported by NIH grants 1R01AA018857-01, 5R21AA025470, P50AA11999 (Animal Core, Morphology Core, and Pilot Project Program), R24AA012885 (Non-Parenchymal Liver Cell Core) and pilot project funding (5P30DK048522-13)." @default.
• W3012226795 created "2020-03-23" @default.
• W3012226795 creator A5070288633 @default.
• W3012226795 date "2020-05-01" @default.
• W3012226795 modified "2023-10-17" @default.
• W3012226795 title "Cell fate, metabolic reprogramming and lncRNA of tumor-initiating stem-like cells induced by alcohol" @default.
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• W3012226795 doi "https://doi.org/10.1016/j.cbi.2020.109055" @default.
• W3012226795 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7238551" @default.
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