| Literature DB >> 30989726 |
Shan-Shan Yao1, Lei Han2, Zi-Bin Tian3, Ya-Nan Yu3, Qi Zhang3, Xiao-Yu Li3, Tao Mao3, Lin Yang3.
Abstract
Celastrol could inhibit cancer cell growth in vitro. However, effect(s) of celastrol on gastric cancer is not well studied. Therefore, we investigated the effects of celastrol on human gastric cancer cell line MKN45 and the underlying mechanisms. We found that celastrol inhibited cell proliferation, migration, and invasion and induced cell apoptosis and G2/M cell cycle arrest (p < .05, p < .01, or p < .001). Under celastrol treatment, overexpression of microRNA-21 (miR-21) increased cell viability, migration, and invasion and inhibited cell apoptosis compared with negative control (p < .05, p < .01, or p < .001). In addition, the phosphorylation of PTEN was significantly up-regulated, whereas PI3K, AKT, p65, and IκBα phosphorylation was statistically decreased by celastrol (p < .05 or p < .01) and then further reversed by miR-21 overexpression (p < .05 or p < .01). On the other side, miR-21 silence showed contrary results (p < .05) as relative to miR-21 overexpression. In conclusion, celastrol inhibits proliferation, migration, and invasion and inactivates PTEN/PI3K/AKT and nuclear factor κB signaling pathways in MKN45 cells by down-regulating miR-21.Entities:
Keywords: NF-κB; PTEN/PI3K/AKT; celastrol; gastric cancer; miR-21
Mesh：
Substances：
Year: 2019 PMID： 30989726 DOI： 10.1002/ptr.6359
Source DB: PubMed Journal: Phytother Res ISSN： 0951-418X Impact factor: 5.878