辣椒素在 B16F10 細胞株引發細胞自噬及細胞凋亡

Abstract

Melanoma is a malignant tumor of melanocytes. If melanoma is found at early stage, it can be removed completely by surgery and the chance of cure is high. Unfortunately, if it is diagnosed late it may lead to skin cancer-relatred death. The treatments to melanoma these days include chemo- and immunotherapy, and radiation therapy. Capsaicin has an anti-proliferative effect in vitro on prostate, colon, gastric, hepatic and leukemic cancer cell lines. It is demonstrated that capsaicin inhibited melanoma cacncer cell lines, however, most of the mechanisms are still unclear. In this study, we used rat melanoma cell line, B16F10, for the evaluation of the anticancer effect of capsaicin . We found that the percentage of apoptosis and changes of mitochondrial membrane potential are notably increased in high concentration of capsaicin (400 μM). Western blot also shows that high concentration of capsaicin decreases Bcl-2 protein. Low concentrations of capsaicin are found to not to activate PARP (Poly ADP ribose polymerase) resulting in no apoptosis. While oxidative stress is not significantly different among different concentrations of capsaicin. We suggest that high concentration of capsaicin might induce apoptosis in B16F10 through mitochondrial dependent pathway. We also found that low concentrations of capsaicin (10, 100 μM) result in autophagy induction in B16F10 cells. Western blot also shows that high concentration of capsaicin increases the level of mTOR phosphorylation. On the other hand, low concentrations of capsaicin increase beclin-1 and autophagy. We suggest that capsaicin-mediated autophagy may involved in cell survival mechanism in B16F10 cells. Thus, we propose to utilize inhibitors of autophagy to examine the percentage of apoposis in B16F10. Similarly, inhibitors of apoptosis will be used to study the autophagy mechanism in B16F10 cells, with the hope to find out the relationship between autophagy and apoptosis in capsaicin-exposed B16F10 cells.