Background and purpose: Salidroside, extracted from Rhodiola rosea, has been reported to possess anti-tumor effect. However, the therapeutic effects of Salidroside on bladder cancer have not been investigated. This study focused on the effects and possible mechanisms of Salidroside on human bladder cancer in vitro. Methods: The human bladder cancer cell line, T24, was incubated with various concentrations of Salidroside (12.5, 25 and 50 ug/ mL) for 24 hours, followed by serial biological examinations. Cell viability, proliferation and toxicity were accessed by MTT, trypan blue exclusion assay and LDH assay. Cell migration was accessed by wound healing assay. ELISA, western blot and immunofluorescence staining were used to detect the expression of TGF β1/smad signaling related proteins and epithelial- mesenchymal transition (EMT). Results: Salidroside treatment of T24 cells significantly inhibited cell proliferation and cell migration. In addition, Salidroside significantly reduced the expression of TGF-β1 and downstream signaling in T24 cells. TGF-β1 downstream signal regulators Smad 2/3 was reduced, while the inhibitor Smad 7 was increased. Further investigating the EMT markers was performd, which showed that Salidroside decreased EMT through decreasing the expression of α-SMA and increasing expression of E-cadherin. Conclusion: In the present study, Salidroside was found to show anticancer effects on bladder cancer T24 cells. These effects were demonstrated by suppressing cell proliferation, tumor invasion and EMT. The underlying mechanisms may be associated with modulating EMT process by down-regulating TGF β1/Smad pathway
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