Salidroside induces apoptosis in human ovarian cancer SKOV3 and A2780 cells through the p53 signaling pathway.

Abstract

Salidroside is one of the most potent compounds extracted from the plant Rhodiola rosea, and its cardiovascular protective effects have been studied extensively. However, the role of salidroside in human ovarian carcinoma remains unknown. The aim of the current study was to investigate the effects of salidroside on the proliferation and apoptosis of SKOV3 and A2780 cells using MTT assay and acridine orange/ethidium bromide staining. Salidroside activated caspase-3 and upregulated the levels of apoptosis-inducing factor, Bcl-2-associated X and Bcl-2-associated death promoter (Bad) proteins. Furthermore, salidroside downregulated the levels of Bcl-2, p-Bad and X-linked inhibitor of apoptosis proteins. Salidroside activated the caspase-dependent pathway in SKOV3 and A2780 cells, upregulating p53, p21Cip1/Waf1 and p16INK4a. These results suggest that the p53/p21Cip1/Waf1/p16INK4a pathway may serve a key function in salidroside-mediated effects on SKOV3 and A2780 cells. The current findings indicate that salidroside may be a promising novel drug candidate for ovarian cancer therapy.