Anticancer effect of salidroside reduces viability through autophagy/PI3K/Akt and MMP-9 signaling pathways in human bladder cancer cells.

Salidroside has a wide range of pharmacological activities, including antitumor, anti-inflammatory, analgesic, antibacterial, antiviral and anti-fertility abilities. In the present study, the effects of salidroside on the viability and apoptosis of bladder cancer cells, and the potential underlying mechanisms, were examined. In the present study, treatment with salidroside reduced cell viability, and induced apoptosis and caspase-9/3 activation in the T24 human bladder carcinoma cell line. Salidroside induced autophagy, promoted the protein expression of nucleoporin p62 and the microtubule-associated proteins 1A/1B light chain 3B, suppressed phosphoinositide 3-kinase (PI3K) and phosphorylated protein kinase B (p-Akt) expression, inhibited matrix metalloproteinase-9 (MMP-9) expression and increased that of Bcl-2-associated X protein, which functions as an apoptosis regulator in T24 cells. In the present study, it was demonstrated that the effect of salidroside reduced the viability and induced the apoptosis of bladder cancer cells through the autophagy/PI3K/Akt and MMP-9 signaling pathways.