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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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B cell translocation gene 1 contributes to antisense Bcl-2-mediated apoptosis in breast cancer cells.

The antiapoptotic protein Bcl-2 is overexpressed in a majority of breast cancers, and is associated with a diminished apoptotic response and resistance to various antitumor agents. Bcl-2 inhibition is currently being explored as a possible strategy for sensitizing breast cancer cells to standard chemotherapeutic agents. Antisense Bcl-2 oligonucleotides represent one method for blocking the antiapoptotic effects of Bcl-2. In this study, we show that antisense Bcl-2 efficiently blocks Bcl-2 expression, resulting in the apoptosis of breast cancer cells. Antisense Bcl-2-mediated cytotoxicity was associated with the induction of the B cell translocation gene 1 (BTG1). Importantly, knockdown of BTG1 reduced antisense Bcl-2-mediated cytotoxicity in breast cancer cells. Furthermore, BTG1 expression seems to be negatively regulated by Bcl-2, and exogenous expression of BTG1 induced apoptosis. These results suggest that BTG1 is a Bcl-2-regulated mediator of apoptosis in breast cancer cells, and that its induction contributes to antisense Bcl-2-mediated cytotoxic effects.[1]

References

  1. B cell translocation gene 1 contributes to antisense Bcl-2-mediated apoptosis in breast cancer cells. Nahta, R., Yuan, L.X., Fiterman, D.J., Zhang, L., Symmans, W.F., Ueno, N.T., Esteva, F.J. Mol. Cancer Ther. (2006) [Pubmed]
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