期刊
FRONTIERS IN ONCOLOGY
卷 11, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fonc.2021.666549
关键词
fangchinoline (FCL); esophageal squamous cell carcinoma (ESCC); cell cycle; intrinsic apoptosis; extrinsic apoptosis
类别
资金
- National Natural Science Foundation of China [81820108022, 81625018, 81602072, 81902380]
- Innovation Program of Shanghai Municipal Education Commission [2019-01-07-00-10-E00056]
- Program of Shanghai Academic/Technology Research Leader [18XD1403800]
The study illustrated the significant growth inhibition of esophageal squamous cell carcinoma (ESCC) by fangchinoline (FCL) through inducing cell cycle arrest and activating apoptosis pathways. FCL demonstrated its potential as an anti-ESCC agent by elucidating its tumor-suppressive efficacy and mechanisms.
Esophageal squamous cell carcinoma (ESCC) is a recalcitrant cancer. The Chinese herbal monomer fangchinoline (FCL) has been reported to have anti-tumor activity in several human cancer cell types. However, the therapeutic efficacy and underlying mechanism on ESCC remain to be elucidated. In the present study, for the first time, we demonstrated that FCL significantly suppressed the growth of ESCC both in vitro and in vivo. Mechanistic studies revealed that FCL-induced G1 phase cell-cycle arrest in ESCC which is dependent on p21 and p27. Moreover, we found that FCL coordinatively triggered Noxa-dependent intrinsic apoptosis and DR5-dependent extrinsic apoptosis by transactivating ATF4, which is a novel mechanism. Our findings elucidated the tumor-suppressive efficacy and mechanisms of FCL and demonstrated FCL is a potential anti-ESCC agent.
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