Light-activated indole-3-acetic acid induces apoptosis in G361 human melanoma cells

초록

Indole-3-acetic acid (IAA) activation by horseradish peroxidase (HRP) has been suggested as a new cancer therapy. Interestingly, we found that ultraviolet B (UVB) radiation also can activate IAA and produce free radicals in a dose-dependent manner. In this study, we attempted to identify the free radicals generated by UVB-irradiated IAA (IAA(UVB)), and to determine whether IAA(UVB) can induce the apoptosis of G361 human melanoma cells. Since IAA/HRP produces reactive oxygen species (ROS), we examined whether IAA(UVB)-generated radicals include ROS. Our results show that IAA(UVB)-induced free radical production is not inhibited by catalase, superoxide dismutase, or sodium formate, indicating that ROS are not generated by IAA UVB. On the other hand, IAA(UVB) caused lipid peroxidation, and this was blocked by Trolox, a water-soluble vitamin E derivative. Moreover, we found that IAA UVB caused apoptotic cell death and that this was inhibited by a low temperature. We further investigated IAA(UVB)-mediated apoptotic pathways, and found that IAA(UVB) causes caspase-8, Bid, caspase-3 activation, and poly (ADP-ribose) polymerase (PARP) cleavage. In addition, these apoptotic pathways were also blocked by low temperature. From these results, we propose that IAA(UVB)-induced free radicals cause human melanoma cell apoptosis via a death receptor-mediated apoptotic pathway.

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