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.