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BEX2 regulates mitochondrial apoptosis and G1 cell cycle in breast cancer by Ali Naderi; Ji Liu; Ian C. Bennett is a Medicine article available to read on EtoBox.
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## Abstract We have recently demonstrated that BEX2 is differentially expressed in primary breast tumors and BEX2 expression is required for the Nerve Growth factor inhibition of ceramide‐induced apoptosis in breast cancer. In this study we investigate the functional role of BEX2 in the survival and growth of breast cancer cells. We demonstrate that BEX2 downregulation induces mitochondrial apoptosis and sensitizes breast cancer cells to the pro‐apoptotic effects of ceramide, doxorubicin and staurosporine. In addition, BEX2 overexpression protects the breast cancer cells against mitochondrial apoptosis. We show that this effect of BEX2 is mediated through the modulation of Bcl‐2 protein family, which involves the positive regulation of anti‐apoptotic member Bcl‐2 and the negative regulation of pro‐apoptotic members BAD, BAK1 and PUMA. Moreover, our data suggests that BEX2 expression is required for the normal cell cycle progression during G1 in breast cancer cells through the regulation of cyclin D1 and p21. To further support the significance of BEX2 in the pathogenesis of breast cancer we demonstrate that BEX2 overexpression is associated with a higher activation of the Bcl‐2/NF‐
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- Author
- Ali Naderi; Ji Liu; Ian C. Bennett
- Publisher
- John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley; Research Square; Test accounts (ISSN 0020-7136)
- Published
- 2010
- Language
- EN
- Field
- Medicine (Health Sciences)