Abstract：
Capsaicin (CAP), extracted from Capsicum fruits, has been reported to exhibit antitumor effects in various lines of cancer cells. However, the mechanism underlying its antitumor efficiency is not fully understood. Autophagy is a fundamental self-degradation process of cells that maintains homeostasis and plays a controversial role in tumor initiation and progression. The EMT is defined as a system regulating cells transformed from an epithelial-like phenotype into a mesenchymal phenotype by several internal and external factors, following the metastatic performance of the cells developed. The present study aimed to investigate the potential role of autophagy in CAP-induced antitumor effects in renal cell carcinoma (RCC) 786-O and CAKI-1 cell lines. The results revealed that CAP remarkably inhibited the migration and invasion of RCC cells in vitro and metastasis in vivo. Moreover, we found that the CAP treatment increased the formation of autophagolysosome vacuoles and LC3 yellow and red fluorescent puncta in RCC cells and upregulated the expression of LC3, suggesting that autophagy was induced by CAP in 786-O and CAKI-1 cell lines. Our further results demonstrated that CAP-induced autophagy was mediated by the AMPK/mTOR pathway. In conclusion, our study provides new knowledge of the potential relationship between autophagy and metastasis inhibition induced by CAP, which might be a promising therapeutic strategy in RCC.
摘要：
辣椒素(CAP),从辣椒果实中提取，据报道，在各种癌细胞系中表现出抗肿瘤作用。然而,其抗肿瘤功效的潜在机制尚不完全清楚。自噬是细胞维持稳态的基本自我降解过程，在肿瘤发生和发展中起着有争议的作用。EMT被定义为通过多种内部和外部因素调节细胞从上皮样表型转化为间充质表型的系统。随着细胞的转移性能发展。本研究旨在探讨自噬在CAP诱导的肾细胞癌（RCC）786-O和CAKI-1细胞系中的潜在作用。结果表明，CAP对体外培养的RCC细胞的迁移、侵袭和体内转移均有明显的抑制作用。此外，我们发现CAP处理增加了RCC细胞中自噬溶酶体液泡和LC3黄色和红色荧光点的形成，并上调了LC3的表达，表明CAP在786-O和CAKI-1细胞系中诱导了自噬。我们的进一步结果表明，CAP诱导的自噬是由AMPK/mTOR通路介导的。总之,我们的研究提供了关于自噬与CAP诱导的转移抑制之间潜在关系的新知识，这可能是RCC的一种有希望的治疗策略。
