Capsaicin induces apoptosis and autophagy in human melanoma cells

辣椒素诱导人类黑色素瘤细胞凋亡和自噬

阅读:9
作者:Haihan Chu, Meng Li, Xiuchun Wang

Abstract

Melanoma is the most lethal type of skin cancer; rapid metastasis and resistance to conventional radio- and chemotherapy make melanoma the most aggressive type of skin cancer. In addition, there is a high recurrence rate within 1 year among patients with melanoma following traditional treatment by chemotherapy or immunotherapy, and these treatment options are only useful in advanced stages. As the efficiency of treatment options for melanoma is not ideal, the present study aimed to confirm that capsaicin has inhibitory effects on the human melanoma A375 and C8161 cell lines in vitro. Capsaicin, the active component of peppers, has been reported to possess substantial anticarcinogenic and antimutagenic activities. Additionally, capsaicin exhibits an inhibitory effect on tumor growth in numerous malignant cell lines. In the present study, flow cytometry, fluorescent puncta detection and western blotting were performed. The experimental results indicated that capsaicin activated apoptosis, and that apoptosis induction was associated with poly(ADP-ribose) polymerase (PARP) cleavage and activation of caspase-3. Additionally, the formation of autophagosomes and accumulation of microtubule-associated proteins 1A/1B light chain 3B-II and beclin 1 suggested that capsaicin induced autophagy in human melanoma cells. Furthermore, inhibiting capsaicin-induced autophagy promoted the activation of cleaved caspase-3 and PARP proteins, which are associated with apoptosis. In addition, inhibition of autophagy using 3-MA enhanced capsaicin-induced cell death, indicating that capsaicin-induced autophagy is a pro-survival process in cells. In conclusion, the results of the present study revealed that capsaicin induced cell apoptosis and autophagy in human melanoma cells and capsaicin may be considered as a novel candidate drug for melanoma treatment.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。