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Bcl-w promotes cell invasion by blocking the invasion-suppressing action of Bax

Title
Bcl-w promotes cell invasion by blocking the invasion-suppressing action of Bax
Authors
Kim E.M.Kim J.Park J.K.Hwang S.-G.Kim W.-J.Lee W.-J.Kang S.W.Um H.-D.
Ewha Authors
이원재강상원
SCOPUS Author ID
강상원scopus
Issue Date
2012
Journal Title
Cellular Signalling
ISSN
0898-6568JCR Link
Citation
vol. 24, no. 6, pp. 1163 - 1172
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
The Bcl-2 family members are key regulators of cellular viability, either promoting or suppressing cell death. Recent reports have indicated that the pro-survival members (Bcl-w, Bcl-X L, and others) also enhance the migratory and invasive potentials of cancer cells, although the mechanisms underlying this phenomenon have yet to be adequately elucidated. Herein, by using human cancer cells and mouse embryonic fibroblasts, we demonstrate that Bcl-w functions in the mitochondria to increase the levels of reactive oxygen species (ROS), which subsequently stimulates the invasion-promoting signaling pathway. By way of contrast, Bax, a member of the multidomain pro-apoptotic group (Bax and Bak), was found to reduce ROS levels, thereby suppressing cell invasion. Analyses of the functional relationship between Bcl-w and Bax have shown that Bcl-w requires Bax for promoting cell invasion, whereas Bax suppresses cell invasion in a Bcl-w-independent manner. By using a Bcl-w mutant (Bcl-w/G94A) that was found not to bind to Bax, we have further determined that Bcl-w should bind to Bax to promote cell invasion. Overall, the results indicate that Bcl-w enhances cellular invasiveness by binding to Bax and subsequently blocking its invasion-suppressing actions. Moreover, these functions of Bcl-w and Bax are mimicked by other pro-survival and pro-apoptotic members, such as Bcl-X L and Bak, respectively. We propose the balance between pro-survival and multidomain pro-apoptotic members as a novel determinant of cellular invasiveness. © 2012 Elsevier Inc..
DOI
10.1016/j.cellsig.2012.01.019
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일반대학원 > 바이오융합과학과 > Journal papers
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