Curcumin inhibits migration and invasion of lung cancer PC-9 cells via down-regulation of nectin-4 expression
10.3969/j.issn.1000-4718.2017.02.013
- VernacularTitle:姜黄素通过下调 nectin-4抑制肺癌PC-9细胞的迁移和侵袭
- Author:
Jun CHEN
;
Demin JIAO
;
Xiali TANG
;
Jian WANG
;
You LI
;
Qingyong CHEN
- Keywords:
Curcumin;
Lung cancer;
Cell migration;
Cell invasion;
Nectin-4
- From:
Chinese Journal of Pathophysiology
2017;33(2):271-277
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the effects of curcumin on the abilities of migration and invasion in the lung cancer PC-9 cells, and to observe the relationship between curcumin and nectin-4 expression.METHODS:The viability, migration and invasion of lung cancer PC-9 cells treated with curcumin or transfected with siNectin-4 were measured by MTT assay, wound healing test and Transwell assay , respectively.The protein levels of nectin-4, p-AKT and AKT in the PC-9 cells treated with curcumin or transfected with siNectin-4 were detected by Western blot .RESULTS:Curcumin in-hibited the viability of PC-9 cells.The wound healing rates and the numbers of the transmembrane cells in curcumin 10μmol/L and 20 μmol/L groups were decreased compared with control group without curcumin treatment .The expression level of nectin-4 was reduced after curcumin treatment for 24 h.The viability of the PC-9 cells was significantly inhibited after transfected with siNectin-4 for 48 h or 72 h (P<0.01), and the wound healing rates was decreased in siNectin-4 group compared with NC group (P<0.01).The numbers of the transmembrane cells in siNectin-4 group was significantly reduced (P<0.01).Curcumin and knockdown of nectin-4 suppressed the activation of AKT pathway in PC-9 cells.In si-Nectin-4+curcumin group , the cell viability reduced compared with curcumin group , and wound healing rates , cell inva-sive ability and AKT phosphorylation levels were decreased .CONCLUSION:Curcumin inhibits migration and invasion of the lung cancer PC-9 cells via down-regulation of nectin-4 expression and inhibition of AKT pathway .
