Nicotine increases the resistance of lung cancer cells to cisplatin through enhancing Bcl-2 stability

摘要: Nicotine is able to activate mitogenic signalling pathways, which promote cell growth or survival as well increase chemoresistance of cancer cells. However, the underlying mechanisms are not fully understood. In this study, we used immunoblotting and immunoprecipitation methods test ubiquitination degradation Bcl-2 affected by nicotine in lung Apoptotic assay was also measure antagonising effect on cisplatin-mediated cytotoxicity. We demonstrated that addition greatly attenuated degradation, further desensitised cells cisplatin-induced process, persistently phosphorylated cotreated with cisplatin. Furthermore, Akt proven be responsible for sustained activation nicotine, antagonised apoptotic signalling. Our study suggested activates its downstream interfere process prevent from being degraded cells, resulting chemoresistance.