Bladder cancer is believed to arise after a series of progressive pathological changes. Cell differentiation exists in almost all cells, when become aberrant, can initiate or promote diseases processes and tumorigenesis. Epithelial-mesenchymal transition (EMT) is a crucial pathophysiological process in cancer initiation and development. Tobacco smoke is an important risk factor of bladder cancer. However, the molecular mechanisms of tobacco smoke-triggered abnormal cell differentiation and EMT in bladder tissues have not been well defined. The current study was designed to investigate the regulatory role of AP-1 in tobacco smoke-triggered urocystic abnormal cell differentiation and EMT in vivo. Exposure of male BALB/c mice to tobacco smoke for 12 weeks altered the expression of cell differentiation and EMT markers in bladder tissues. Importantly, we demonstrated that AP-1 modulated tobacco smoke-induced abnormal cell differentiation and EMT, as evidenced by the findings that tobacco smoke elevated AP-1 activation, and tobacco smoke-mediated cell differentiation and EMT were reversed by AP-1 suppression. These data indicated that AP-1 play an important role in tobacco smoke-induced urocystic abnormal cell differentiation and EMT. These findings provide new insights into the mechanism of tobacco smoke associated urocystic tumorigenesis and may help to discover potential targets for novel therapies and chemoprevention.
Keywords: AP-1; EMT; Tobacco smoke; abnormal cell differentiation; bladder cancer.
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