Gamma Secretion Inhbitors Block Notch Signaling Pathway On Bladder Cancer Epithelial-mesenchymal Transformation (EMT) Effect

Objective： To explore the Notch signaling pathway in bladder cancerEpithelial-mesenchymal transformation (EMT) and its molecular mechanism.Methods： Gamma-secretase inhibitors on human bladder cancer cell lines,T24,5637,J82-cell growth and morphology change is observed by invertedmicroscope. RT-PCR and Western blot is respectively used to detect the changes ofthe human bladder cancer cell lines, T24,5637,J82EMT in molecular markers ofE-cadherin, N-cadherin, Vimentin, Alpha-smooth muscle actin before and after theyare disposed by gamma secretion inhibitors. Gamma-secretase inhibitors on humanbladder cancer cell lines, T24,5637,J82-cell drug resistance change is detected andanalyzed by MTT colorimetric method. Meanwhile, transwell is used to detect thechange of T24,5637,J82human bladder cancer cells’ invasive ability before and afterthey are disposed by gamma secretion inhibitors.Results：RT-PCR and Western blot shows that the Gamma-Secretase Inhibitorsfor treatment of EMT standard E-cadherin is regulated up after (P<0.05), andN-cadherin, Vimentin, Alpha-smooth muscle actin is regulated down (P<0.05). MTTshows that the cell growth of human bladder cancer cell lines, T24,5637,J82isobviously repressed after being disposed by Gamma-Secretase Inhibitors. Transwelltesting shows that the bladder cancer cell lines,T24,5637,J82posterity which gothrough the porous membrane of cells is significantly reduced (P<0.05) after disposedby Gamma-secretase inhibitors.Conclusion：Gamma-Secretase Inhibitors can significantly inhibit the growth ofhuman bladder cancer cells and Notch signaling pathway is blocked the EMTmolecular markers in bladder cancer cells after E-cadherin up, N-cadherin, Vimentin,Alpha-smooth muscle actin expression reduction inhibition of EMT, affecting thegrowth and invasiveness of bladder cancer cells, drug resistance.