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Bcl‐w promotes cell invasion by inducing mitochondrial ROS production
Author(s) -
Um HongDuck,
Kim Eun Mi
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.930.15
Subject(s) - microbiology and biotechnology , mitochondrion , downregulation and upregulation , apoptosis , cancer cell , biology , embryonic stem cell , protein kinase b , function (biology) , pi3k/akt/mtor pathway , signal transduction , cancer , gene , genetics
Bcl‐w, a member of the Bcl‐2 family, acts in the mitochondria to block apoptosis. We have previously shown that the upregulation of Bcl‐w in cancer cells also enhances their migratory and invasive potentials by stimulating signaling components, such as phosphoinositide 3‐kinase and Akt. To better understand the mechanism underlying this new function of Bcl‐w, we deleted its C‐terminal hydrophobic tail. This treatment abolished the ability of Bcl‐w to localize in the mitochondria and promote cell invasion, suggesting that Bcl‐w requires its mitochondrial localization for enhancing cellular invasiveness. It was also found that Bcl‐w stimulates mitochondrial ROS production, which then mediates the ability of Bcl‐w to induce the invasion pathway. All these results were obtained using either human cancer cells or mouse embryonic fibroblasts. Therefore, it appears that ROS are involved in Bcl‐w‐induced invasion not only in cancer but also normal cells as well as in both human and mouse cells.