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

Enhanced sensitivity to cytochrome c- induced apoptosis mediated by PHAPI in breast cancer cells.

Apoptotic signaling defects both promote tumorigenesis and confound chemotherapy. Typically, chemotherapeutics stimulate cytochrome c release to the cytoplasm, thereby activating the apoptosome. Although cancer cells can be refractory to cytochrome c release, many malignant cells also exhibit defects in cytochrome c-induced apoptosome activation, further promoting chemotherapeutic resistance. We have found that breast cancer cells display an unusual sensitivity to cytochrome c-induced apoptosis when compared with their normal counterparts. This sensitivity, not observed in other cancers, resulted from enhanced recruitment of caspase-9 to the Apaf-1 caspase recruitment domain. Augmented caspase activation was mediated by PHAPI, which is overexpressed in breast cancers. Furthermore, cytochrome c microinjection into mammary epithelial cells preferentially killed malignant cells, suggesting that this phenomenon might be exploited for chemotherapeutic purposes.[1]


  1. Enhanced sensitivity to cytochrome c-induced apoptosis mediated by PHAPI in breast cancer cells. Schafer, Z.T., Parrish, A.B., Wright, K.M., Margolis, S.S., Marks, J.R., Deshmukh, M., Kornbluth, S. Cancer Res. (2006) [Pubmed]
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