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  • Title: Involvement of c-Myc in growth inhibition of Hep 3B human hepatoma cells by a vitamin K analog.
    Author: Ge L, Wang Z, Wang M, Kar S, Carr BI.
    Journal: J Hepatol; 2004 Nov; 41(5):823-9. PubMed ID: 15519656.
    Abstract:
    BACKGROUND/AIMS: A synthetic vitamin K analog, compound 5 (Cpd 5), is a potent inhibitor of cell growth. The aim was to investigate whether c-Myc was involved in Cpd 5-induced cell growth inhibition. METHODS: Human hepotoma cells (Hep 3B) were cultured and treated with Cpd 5, and c-Myc protein expression and phosphorylation were investigated using Western blot analysis. RESULTS: Cpd 5 was found to inhibit c-Myc protein expression and induce c-Myc phosphorylation in Hep 3B cells. The phosphorylation of c-Myc was induced by both Cpd 5-mediated persistent extracellular signal-regulated kinase (ERK) phosphorylation and Cpd 5 increased glycogen synthase kinase-3 (GSK-3) activity. When using GSK-3 inhibitor, SB216763, c-Myc phosphorylation was significantly decreased and c-Myc levels were restored in Cpd 5 treated cells, suggesting that Cpd 5-mediated increase of GSK-3 activity enhanced c-Myc degradation and resulted in reduction of c-Myc levels. The lower c-Myc levels were found to cause altered expression of two c-Myc target genes, growth arrest gene gadd45 and ornithine decarboxylase (ODC). CONCLUSIONS: The results suggest that Cpd 5-mediated c-Myc phosphorylation resulted in enhanced c-Myc protein degradation and reduced c-Myc protein levels, which may contribute to cell growth inhibition by Cpd 5.
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