Dedifferentiation of human hepatocytes by extracellular matrix proteins in vitro: quantitative and qualitative investigation of cytokeratin 7, 8, 18, 19 and vimentin filaments
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2019, EBioMedicineCitation Excerpt :Following disease progression and subsequent functional failure, parenchymal cells, which are primarily responsible for maintaining organ function, lose their key identity genes [9,10,13]. Moreover, clinical and experimental observations indicate that loss of hepatocyte identity may be associated with the development of cirrhosis of various etiologies, or its advanced complications (e.g. hepatocellular carcinoma) [11,14,15]. However, the mechanism of parenchymal dedifferentiation and the underlying molecular basis have yet to be defined.
Hydroxylase Activity of ASPH Promotes Hepatocellular Carcinoma Metastasis Through Epithelial-to-Mesenchymal Transition Pathway
2018, EBioMedicineCitation Excerpt :This is not surprising as most predicted ASPH substrates are extracellular matrix (ECM) proteins [40,41] and membrane ASPH sheds its catalytic domain outside of the membrane, facilitating the hydroxylation of ECM by ASPH. Although vimentin is an intracellular protein, it is actually connected to a complicated ECM network through a physical interaction [42–44]. The interaction between ASPH and vimentin provided a possibility that ECM might relay the inhibitory signal upon FE1 binding to surface ASPH to regulate the vimentin function.
Keratinocyte serum-free medium maintains long-term liver gene expression and function in cultured rat hepatocytes by preventing the loss of liver-enriched transcription factors
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