Cyr61 Expression Confers Resistance to Apoptosis in Breast Cancer MCF-7 Cells by a Mechanism of NF-κB-dependent XIAP Up-Regulation

We showed that stable cell lines overexpressing Cysteine-rich 61 had acquired a remarkable resistance to apoptosis induced by paclitaxel, adriamycin, and ␤-lapachone

Ming-Tsan Lin; Cheng-Chi Chang; Szu-Ta Chen; Huei-Ling Chang; Jen-Liang Su; Yat-Pang Chau; Min-Liang Kuo

2004

Scholarcy highlights

  • Apoptosis is a genetically controlled process that plays an essential role in embryogenesis, homeostasis, and the cellular response to stressful stimuli
  • In this study we investigate whether overexpression of Cyr in breast cancer MCF-7 cells could modulate their sensitivity to apoptosis induced by various anti-cancer drugs
  • We found that NF-␬B was constitutively activated in Cysteine-rich 61-overexpressing breast cancer cells and was required for these cells to be resistant to anti-cancer drug-induced apoptosis
  • NF-␬B Is Critical for Cyr61-mediated Anti-apoptosis—We further explored whether NF-␬B activation is involved in the Cyr61-mediated anti-apoptotic effect in breast cancer MCF-7 cells
  • Cyr has been shown to augment activity in endothelial cells by an unknown mechanism, and this might account in part for its angiogenic effect
  • In agreement with other studies, we have shown here that overexpression of Cyr significantly increases the resistance of MCF-7 cells to doxorubicin, paclitaxel, and ␤-lapachone but not to topotecan and etoposide
  • Stable overexpression of Cyr increased MCF-7 cells resistance to some anti-cancer drug-induced apoptosis

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