Matches in SemOpenAlex for { <https://semopenalex.org/work/W2897301109> ?p ?o ?g. }
- W2897301109 abstract "Abstract Hepatocyte nuclear factor 4 alpha (HNF4α) is a master regulator of liver-specific gene expression with potent tumor suppressor activity, yet many liver tumors express HNF4α. This study reveals that P1-HNF4α, the predominant isoform expressed in the adult liver, inhibits expression of tumor promoting genes in a circadian manner. In contrast, an additional isoform of HNF4α, driven by an alternative promoter (P2-HNF4α), is induced in HNF4α-positive human hepatocellular carcinoma (HCC). P2-HNF4α represses the circadian clock gene ARNTL (BMAL1), which is robustly expressed in healthy hepatocytes, and causes nuclear to cytoplasmic re-localization of P1-HNF4α. We reveal mechanisms underlying the incompatibility of BMAL1 and P2-HNF4α in HCC, and demonstrate that forced expression of BMAL1 in HNF4α-positive HCC prevents the growth of tumors in vivo. These data suggest that manipulation of the circadian clock in HNF4α-positive HCC could be a tractable strategy to inhibit tumor growth and progression in the liver." @default.
- W2897301109 created "2018-10-26" @default.
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- W2897301109 date "2018-10-19" @default.
- W2897301109 modified "2023-10-17" @default.
- W2897301109 title "Incompatibility of the circadian protein BMAL1 and HNF4α in hepatocellular carcinoma" @default.
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- W2897301109 doi "https://doi.org/10.1038/s41467-018-06648-6" @default.
- W2897301109 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6195513" @default.
- W2897301109 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30341289" @default.
- W2897301109 hasPublicationYear "2018" @default.
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