RU 21. Down - regulation of Id-1 in bladder cancer cells can increase the cellular chemosensitivity and epirubicin - induced apoptosis

Objective: To investigate the role of Inhibitor of differentiation (Id-1) down-regulation in the chemosensitivity of bladder cancer cells, and the effect of Id-1 suppression on chemotherapeutic drug induced apoptosis in bladder cancer cells.

Methods: The Id-1 si-RNA vector was generated and transfected into MGH-U1 cells. Stable si-Id-1 transfectants and vector control clones were generated. MTT assay and colony forming assy were performed to compare the chemosensitivity of si-Id-1 transfectants and vector control. Type I collagen invasion assay was used to detect the invasive ability of different clones. The expression levels of apoptosis related proteins were analyzed by Western blotting to study the effect of Id-1 suppression on anticancer drug-induced apoptosis.

Results: After generation of the stable Id-1 down-regulation transfectants successfully, the results of MTT assay and colony forming assay showed down-regulation of Id-1 could increase cellular sensitivity to epirubicin. Type I collagen invasion assay showed less percentage of the si-Id-1 cells than vector cells could invade into extracellular matrix. Furthermore, the analysis of apoptosis related protein revealed that down-regulation of Id-1 leaded to increased expression of cleaved PARP and cleaved Caspase 3, which support the negative role of Id-1 in epirubicin induced apoptosis.

Conclusions: Results in this study suggest that down-regulation of Id-1 could increase cellular chemosensitivity to epirubicin by increased anticancer drug induced apoptosis.