Studies on the mechanism of arsenic trioxide-induced apoptosis in HepG 2 human hepatocellular carcinoma cells

Objective To study the anti-tumor effect of arsenic trioxide on the HepG 2 human hepatocellular carcinoma cell line, and to explore its mechanism of action. Methods The MTT assay was used to determine the inhibitory effect of As 2 O 3 on HepG 2 cells at various As 2 O 3 concentrations. The expression of p-JNK, caspase-3 and PARP was detected by Western blots. Results As 2 O 3 markedly inhibited the growth of the HepG 2 cells and induced apoptosis. The results of Western blot analysis showed that the As 2 O 3 -induced apoptosis was accompanied by caspase-3 and PARP activation. p-JNK was detected at 10 min following As 2 O 3 treatment, and preceded to peak at 20 min, and decreased by 30 min. The total protein content did not obviously change. The activation of JNK occurred prior to cell apoptosis. SP600125, a JNK inhibitor, suppressed the As 2 O 3 -induced activation of caspase-3 and PARP cleavage. Conclusion As 2 O 3 inhibits the proliferation of human HepG 2 hepatocellular carcinoma cells by inducing apoptosis in vitro. As 2 O 3 -induced apoptosis is accessed through the caspase-3 pathway. The JNK signal-transduction pathway and caspase-3 are involved upstream in the As 2 O 3 -induced HepG 2 apoptotic response.