Induction of apoptosis in hepatocellular carcinoma Smmc-7721 cells by vitamin K is associated with p53 and independent of the intrinsic apoptotic pathway.

Autor: Li, Lu, Qi, Zhiling, Qian, Jin, Bi, Fuyong, Lv, Jun, Xu, Lei, Zhang, Ling, Chen, Hongyu, Jia, Renbing
Zdroj: Molecular & Cellular Biochemistry; Sep2010, Vol. 342 Issue 1/2, p125-131, 7p
Abstrakt: Vitamin K (VK) can exert cell growth inhibitory effects in various human cancer cells. In this study, we investigated the cell growth inhibitory effects of VK in hepatocellular carcinoma Smmc-7721 cells and the mechanisms involved. We found that VK-inhibited cell proliferation in Smmc-7721 cells in a dose-dependent manner, and the IC50 of VK in Smmc-7721 cells was 9.73 μM at 24 h. The data from flow cytometric analyses, DNA fragmentation assays, and caspase 3 activity assays revealed that apoptosis was the determining factor in VK activity. Furthermore, a significant increase in p53 phosphorylation and protein level was exhibited in apoptotic cells treated with VK, although there were no changes in p53 mRNA expression. Bax expression was unaffected by VK in Smmc-7721 cells. In addition, our study showed that caspase 3 was activated by caspase 8, not caspase 9, in Smmc-7721 cells treated with VK. In summary, these data suggested that VK can inhibit the growth of Smmc-7721 cells by induction of apoptosis involving caspase 8 activation and p53. This apoptotic process was not mediated by the intrinsic apoptotic pathway. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index
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