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  • Title: Enhanced sensitivity to cytochrome c-induced apoptosis mediated by PHAPI in breast cancer cells.
    Author: Schafer ZT, Parrish AB, Wright KM, Margolis SS, Marks JR, Deshmukh M, Kornbluth S.
    Journal: Cancer Res; 2006 Feb 15; 66(4):2210-8. PubMed ID: 16489023.
    Abstract:
    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.
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