Effect of salvianolic acid A on the proliferation and apoptosis in esophageal cancer cells and the underlying mechanisms. / ä¸¹é šé ¸Aå¯¹é£Ÿç®¡ç™Œç»†èƒžå¢žæ®–ä¸Žå‡‹äº¡çš„å½±å“åŠå ¶æœºåˆ¶.

ABSTRACT

OBJECTIVES: To explore the effect of salvianolic acid A (SalA) on the proliferation and apoptosis in esophageal cancer cell line KYSE-150 and the possible mechanisms. METHODS: The esophageal cancer cells were randomly divided into 4 groups a control group, a 10 µmol/L SalA group, a 25 µmol/L SalA group, and a 50 µmol/L SalA group. Cell counting kit-8 (CCK-8) was used to detect the cell proliferation activity. Flow cytometry was used to detect cell cycle distribution and cell apoptosis rate. Western blotting was used to detect the protein expression of cell proliferation maker Ki-67, cyclin D1, cyclin-dependent kinase 4 (CDK4), CDK6, B-cell lymphoma-2 (Bcl-2), Bcl-2 associated X (Bax), cleaved-caspase-9, cleaved-caspase-3, phosphatidylinositol 3-kinase (PI3K), phosphorylated protein kinase B (p-Akt) and mechanistic target of rapamycin (mTOR). RESULTS: Compared with the control group, the cell proliferation activity was significantly reduced (P<0.01); the cells in the G1 phase were significantly increased, and the S phase cells were significantly reduced (both P<0.01); the cell apoptosis rate was significantly increased (P<0.01) in the SalA groups at different concentration; the expression levels of Ki-67, cyclin D1, CDK4, CDK6, Bcl-2, PI3K, p-Akt and mTOR were decreased significantly, but the expression levels of p21, Bax, cl-caspase-9 and cl-caspase-3 were increased significantly in the SalA groups at different concentration (all P<0.01). CONCLUSIONS: SalA can inhibit the proliferation and induce G1 phase arrest and apoptosis in the esophageal cancer cell line KYSE-150, which may be related to the activation of PI3K/Akt/mTOR signal pathway.