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Disruption of the interaction between PMCA2 and calcineurin triggers apoptosis and enhances paclitaxel-induced cytotoxicity in breast cancer cells
Faculty
Pharmacy
Year:
2012
Type of Publication:
Article
Pages:
2362-2368
Authors:
Mohamed, Tamer M. A, Neyses, Ludwig, Cartwright, Elizabeth J, Oceandy, Delvac, Baggott, Rhiannon R, Holton, Marylouisa, Blanc, Marie Cecile, Roux-Soro, Sandrine C, Brown, Sarah, Brown, James E, Wang, Weiguang, Armesilla, Angel L
DOI:
10.1093/carcin/bgs282
Journal:
CARCINOGENESIS OXFORD UNIV PRESS
Volume:
33
Research Area:
Oncology
ISSN
ISI:000311903500007
Keywords :
Disruption , , interaction between PMCA2 , calcineurin triggers
Abstract:
Cancer is caused by defects in the signalling mechanisms that govern cell proliferation and apoptosis. It is well known that calcium-dependent signalling pathways play a critical role in cell regulation. A tight control of calcium homeostasis by transporters and channel proteins is required to assure a proper functioning of the calcium-sensitive signal transduction pathways that regulate cell growth and apoptosis. The plasma membrane calcium ATPase 2 (PMCA2) has been recently identified as a negative regulator of apoptosis that can play a significant role in cancer progression by conferring cells resistance to apoptosis. We have previously reported an inhibitory interaction between PMCA2 and the calcium-activated signalling molecule calcineurin in breast cancer cells. Here, we demonstrate that disruption of the PMCA2/calcineurin interaction in a variety of human breast cancer cells results in activation of the calcineurin/NFAT pathway, upregulation in the expression of the pro-apoptotic protein Fas Ligand and in a concomitant loss of cell viability. Reduction in cell viability is the consequence of an increase in cell apoptosis. Impairment of the PMCA2/calcineurin interaction enhances paclitaxel-mediated cytotoxicity of breast tumoral cells. Our results suggest that therapeutic modulation of the PMCA2/calcineurin interaction might have important clinical applications to improve current treatments for breast cancer patients.
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