期刊
ANNALS OF TRANSLATIONAL MEDICINE
卷 7, 期 20, 页码 -出版社
AME PUBLISHING COMPANY
DOI: 10.21037/atm.2019.10.07
关键词
Lung cancer; Ecliptasaponin A (ES); apoptosis signal-regulating kinase 1 (ASK1); c-Jun N-terminal kinase (JNK); autophagy; apoptosis
资金
- Key research project of traditional Chinese medicine science and technology plan in Zhejiang Province [2015ZZ007]
- Key discipline of traditional Chinese medicine (integrated traditional Chinese and western medicine) in Zhejiang Province [2017YFC0113500]
Background: Non-small cell lung cancer (NSCLC) is one of the causes of carcinomas mortality worldwide. Ecliptasaponin A (ES), a natural product extracted from the plant known as Eclipta prostrata, has been reported as an anti-cancer drug against various cancer cell lines. However, the exact mechanisms of ES have not yet been fully characterized. Methods: Numerous studies have been done to support that ES has a powerful inhibiting effect on the growth of cancers via the activation of apoptosis and autophagy. TO explore the underlying mechanisms of anti-cancer and investigate the relationships of the apoptosis and autophagy, we used apoptosis signal-regulating kinase 1 (ASK1) inhibitor (GS-4997), c-Jun N-terminal kinase (JNK) inhibitor (SP600125), and autophagy inhibitor [chloroquine (CQ) and 3-methyladenine (3-MA)]. Results: ES could potently suppress cell viability and induces apoptotic cell death of human lung cancer cells H460 and H1975. ES activated apoptosis via ASK1/JNK pathway, GS-4997 and SP600125 can attenuated these effects. Furthermore, ES could triggered autophagy in lung cancer cell lines, and the autophagy inhibitor 3-MA and CQ reversed ES-induced apoptosis in 11460 and H1975 cells. Furthermore, SP600125 can inhibit autophagy. Conclusions: This study showed that ES induces apoptosis in human lung cancer cells by triggering enhanced autophagy and ASK1/JNK pathway, which may thus be a promising agent against lung cancer.
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