Title : ABT737 reverses cisplatin resistance by regulating ER-mitochondria Ca2+ signal transduction in human ovarian cancer cells.

Pub. Date : 2016 Dec

PMID : 27748803






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1 However, the function of Bcl-2 in cisplatin resistance in human ovarian cancer cells is not fully understood. Cisplatin BCL2 apoptosis regulator Homo sapiens
2 In this study, we found that the pharmacological inhibitor ABT737 or genetic knockdown of Bcl-2 increased cisplatin cytotoxicity in cisplatin-resistant ovarian cancer cells. Cisplatin BCL2 apoptosis regulator Homo sapiens
3 In this study, we found that the pharmacological inhibitor ABT737 or genetic knockdown of Bcl-2 increased cisplatin cytotoxicity in cisplatin-resistant ovarian cancer cells. Cisplatin BCL2 apoptosis regulator Homo sapiens
4 Additionally, treatment with ABT737 or Bcl-2 siRNA increased cisplatin-induced free Ca2+ levels in the cytosol and mitochondria, which increased endoplasmic reticulum (ER)-associated and mitochondria-mediated apoptosis. Cisplatin BCL2 apoptosis regulator Homo sapiens
5 In addition, ABT737 or Bcl-2 siRNA increased the ER-mitochondria contact sites induced by cisplatin in cisplatin-resistant SKOV3/DDP ovarian cancer cells. Cisplatin BCL2 apoptosis regulator Homo sapiens
6 In addition, ABT737 or Bcl-2 siRNA increased the ER-mitochondria contact sites induced by cisplatin in cisplatin-resistant SKOV3/DDP ovarian cancer cells. Cisplatin BCL2 apoptosis regulator Homo sapiens
7 Collectively, these results indicate that pharmacological inhibitors or genetic knockdown of Bcl-2 may be a potential strategy for improving cisplatin treatment of ovarian cancer. Cisplatin BCL2 apoptosis regulator Homo sapiens