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

Pub. Date : 2014 Apr 2

PMID : 24548862






6 Functional Relationships(s)
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1 Nicotine increases the resistance of lung cancer cells to cisplatin through enhancing Bcl-2 stability. Nicotine BCL2 apoptosis regulator Homo sapiens
2 METHODS: In this study, we used immunoblotting and immunoprecipitation methods to test the ubiquitination and degradation of Bcl-2 affected by nicotine in lung cancer cells. Nicotine BCL2 apoptosis regulator Homo sapiens
3 RESULTS: We demonstrated that the addition of nicotine greatly attenuated Bcl-2 ubiquitination and degradation, which further desensitised lung cancer cells to cisplatin-induced cytotoxicity. Nicotine BCL2 apoptosis regulator Homo sapiens
4 In this process, Bcl-2 was persistently phosphorylated in the cells cotreated with nicotine and cisplatin. Nicotine BCL2 apoptosis regulator Homo sapiens
5 Furthermore, Akt was proven to be responsible for sustained activation of Bcl-2 by nicotine, which further antagonised cisplatin-mediated apoptotic signalling. Nicotine BCL2 apoptosis regulator Homo sapiens
6 CONCLUSIONS: Our study suggested that nicotine activates its downstream signalling to interfere with the ubiquitination process and prevent Bcl-2 from being degraded in lung cancer cells, resulting in the increase of chemoresistance. Nicotine BCL2 apoptosis regulator Homo sapiens