Title : Nicotine enhances the antiapoptotic function of Mcl-1 through phosphorylation.

Pub. Date : 2009 Dec

PMID : 19903766






8 Functional Relationships(s)
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1 Nicotine enhances the antiapoptotic function of Mcl-1 through phosphorylation. Nicotine MCL1 apoptosis regulator, BCL2 family member Homo sapiens
2 Here, we found that nicotine induces Mcl-1 phosphorylation through activation of extracellular signal-regulated kinase 1/2 in association with increased chemoresistance of human lung cancer cells. Nicotine MCL1 apoptosis regulator, BCL2 family member Homo sapiens
3 Since nicotine stimulates Mcl-1 phosphorylation and survival in cells expressing wild-type but has no such effects in cells expressing T163A Mcl-1 mutant, this indicates that nicotine induces Mcl-1 phosphorylation exclusively at the T163 site and that phosphorylation of Mcl-1 at T163 is required for nicotine-induced survival. Nicotine MCL1 apoptosis regulator, BCL2 family member Homo sapiens
4 Mechanistically, nicotine-induced Mcl-1 phosphorylation significantly enhances the half-life of Mcl-1, which renders Mcl-1 a long-term survival activity. Nicotine MCL1 apoptosis regulator, BCL2 family member Homo sapiens
5 Mechanistically, nicotine-induced Mcl-1 phosphorylation significantly enhances the half-life of Mcl-1, which renders Mcl-1 a long-term survival activity. Nicotine MCL1 apoptosis regulator, BCL2 family member Homo sapiens
6 Mechanistically, nicotine-induced Mcl-1 phosphorylation significantly enhances the half-life of Mcl-1, which renders Mcl-1 a long-term survival activity. Nicotine MCL1 apoptosis regulator, BCL2 family member Homo sapiens
7 Specific depletion of Mcl-1 by RNA interference blocks nicotine-stimulated survival and enhances apoptotic cell death. Nicotine MCL1 apoptosis regulator, BCL2 family member Homo sapiens
8 Thus, nicotine-enhanced survival of lung cancer cells may occur through activation of Mcl-1 by phosphorylation at T163 site, which may contribute to development of human lung cancer and/or chemoresistance. Nicotine MCL1 apoptosis regulator, BCL2 family member Homo sapiens