L-mimosine induces melanoma cell apoptosis through reactive oxygen species and mitochondrial apoptosis pathway

Abstract

Abstract Clinical data have shown that emerging therapies are still not effective in controlling melanoma growth. L-mimosine is known to fight against the growth of various tumors, but the in vitro and in vivo studies of L-mimosine against melanoma are still lacking in detailed studies. In this study, we used MTT assay, plate colony formation assay, and flow cytometry analysis to evaluate the anti-melanoma effect of L-mimosine. The results showed that L-mimosine inhibited melanoma cells (A375 and B16) proliferation by increasing the apoptosis rate. In a mechanistic study, we found that L-mimosine obviously decreased the permeability of mitochondrial membrane by downregulating Bax and upregulating Bcl-2, after which it significantly increased the levels of reactive oxygen species, cytoplasmic cytochrome C, cleaved caspase 9, and cleaved caspase 3, leading to melanoma cell apoptosis. Furthermore, we found that antioxidant NAC obviously counteracted the inhibitory effect of L-mimosine on melanoma cell growth in vitro and in vivo. The results suggested that L-mimosine induced melanoma cell apoptosis through a reactive oxygen species–dependent mitochondrial apoptotic pathway. The results of this study will provide some data and theoretical support for the research on the anti-melanoma mechanism of L-mimosine.