Effect of salinomycin on metastasis and invasion of bladder cancer cell line T24

Objective: To explore the effect of salinomycin on the metastasis and invasion of bladder Cancer cell line T24 by regulating the related protein expression in the process of epithelial-mesenchymal transition (EMT), and to provide experimental basis for the treatment of urological tumors.

Methods: The bladder Cancer cell line T24 was cultured in vitro. The rat bladder tumor model was established in vivo. The rats were randomized into two groups, among which the rats in the experiment group were given intraperitoneal injection of salinomycin, while the rats in the control group were given intraperitoneal injection of normal saline. The change of tumor cells in the two groups was observed. Transwell was used to detect the cell migration and invasion abilities, Real-Time PCR was used to detect the expression of mRNA, while Western-blot was utilized for the determination of the expressions of E-cadherin and vimentin proteins.

Results: The metastasis and invasion abilities of serum bladder Cancer cell line T24 after salinomycin treatment in the experiment group were significantly reduced when compared with those in the control group, and the tumor metastasis lesions were decreased from an average of 1.59 to 0.6 (P < 0.05). T24 cell proliferation in the experiment group was gradually decreasing. T24 cell proliferation at 48 h was significantly lower than that at 12 h and 24 h (P < 0.05). T24 cell proliferation at 24 h was significantly lower than that at 12 h (P < 0.05). T24 cell proliferation at each timing point in the experiment group was significantly lower than that in the control group (P < 0.05). The serum mRNA level and E-cadherin expression in the tumor tissues in the experiment group were significantly higher than those in the control group, while vimentin expression level was significantly lower than that in the control group (P < 0.05).

Conclusions: Salinomycin can suppress the metastasis and invasion of bladder Cancer cells, of which the mechanism is probably associated with the inhibition of EMT of tumor cells.