Liver tumor promotion : effect of phenobarbital on EGF and protein kinase C signal transduction and transforming growth factor-β1 expression
作者： Randy L. Jirtle , Sharon A. Meyer
DOI: 10.1007/BF01297035
关键词:
摘要: Phenobarbital (PB) added to the medium of cultured rat hepatocytes alters epidermal growth factor (EGF) dependent mitogenesis in a biphasic manner; PB concentrations 1 mM) results transient inhibition EGF binding hepatocytes. The kinetics this effect are similar those obtained when exposed phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA), skin tumor promoter and activator Ca2+/phospholipid-dependent protein kinase C. However, several observations suggest that distinct mechanisms mediate responses these two promoters. First, inhibitory effects TPA on additive. Also down-regulation receptors response occurs with hepatocytes, A431 carcinoma cells, HepG2 hepatoma liver epithelial but only sensitive PB. Furthermore, translocation C membrane treated not chronic treatment rats further sensitizes receptor downregulation by inin vitro while desensitizing them TPA. This latter is correlated decreased ability induce membrane. significantly increases intracellular concentration TGF-β1 periportal putative preneoplastic cells. may therefore have an important function regulating early stages cell cycle progression proliferating
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