期刊
ARCHIVES OF PHARMACAL RESEARCH
卷 41, 期 10, 页码 986-994出版社
PHARMACEUTICAL SOC KOREA
DOI: 10.1007/s12272-018-1049-8
关键词
Toxicarioside N; Autophagy; Apoptosis; SGC-7901 cells; Akt; mTOR
资金
- National Natural Science Foundation of China [81560484, 81460557]
- Hainan province natural science foundation of China [817147]
Toxicarioside N (Tox N), a natural product extract from Antiaris toxicaria, has been reported to induce apoptosis in human gastric cancer cells. However, the mechanism and actual role of autophagy in Tox N-induced apoptosis of human gastric cancer cells remains poorly understood. In the current study, we demonstrated that Tox N could induce autophagy by inhibiting the Akt/mTOR signaling pathway in SGC-7901 cells. Moreover, we found that the inhibition of autophagy by 3-methyladenine, an autophagy inhibitor, enhanced Tox N-induced apoptotic cell death. However, the stimulation of autophagy by rapamycin, an autophagy activator, remarkably suppressed Tox N-induced apoptosis, suggesting that autophagy plays a protective role in Tox N-induced apoptosis. Thus, the results from this study suggested that Tox N combination with an autophagy inhibitor might be a promising strategy to enhance the anticancer activity of Tox N for the treatment of human gastric cancer.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据