Salidroside reduces renal cell carcinoma proliferation by inhibiting JAK2/STAT3 signaling

Abstract

Salidroside has been reported to exhibit anticancer properties. This study aimed to investigate the effects of salidroside on renal cell carcinoma growth. Cell viability and proliferation was assessed by Cell Counting Kit-8 and colony formation assays in A498 and 786-0 cells. The effects of salidroside on in vivo tumor growth were also assessed in a mouse xenograft model of renal cell carcinoma. Flow cytometry was used to analyze cell cycle and apoptosis and protein levels were determined by western blotting. Salidroside reduced cell viability and colony formation in both cell lines in a concentration- and time-dependent manner. Tumor growth was also suppressed in the mouse model. Furthermore, salidroside induced significant G1 phase cell cycle arrest and induced apoptosis in both A498 and 786-0 cells. Higher concentrations of salidroside reduced the levels of phosphorylated signal transducer and activator of transcription 3 (STAT3) and Janus kinase 2 (JAK2). These results suggested that salidroside produced potent anticancer properties in renal cell carcinoma by modulating JAK2/STAT3 signaling. Administration of salidroside to patients with renal cell carcinoma might provide a promising therapeutic strategy for this malignancy.

Keywords: JAK2/STAT3; Salidroside; apoptosis; growth; renal cell carcinoma.