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Title of Journal: Breast Cancer Res Treat

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Abbravation: Breast Cancer Research and Treatment

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Springer US

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DOI

10.1007/s00254-007-0762-2

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1573-7217

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Reactive oxygen species induce phosphorylation of

Authors: Gregory E Weitsman Wineeta Weebadda Kanyarat Ung Leigh C Murphy
Publish Date: 2008/10/21
Volume: 118, Issue: 2, Pages: 269-279
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Abstract

Estrogen receptor α ERα is a wellknown target for signaling pathways originating from growth factor receptors Reactive oxygen species ROS can induce activation of extracellular response kinase 1/2 Erk1/2 and protein kinase B Akt Both kinases have been implicated in the phosphorylation of serine 118 and serine 167 on ERα respectively This activity may lead either to ligandindependent activation of ERα or downregulation of ERα and may contribute to development of the resistance to endocrine therapy Treatment of MCF7 human breast cancer cells with glucose oxidase GO 01 un/ml induced transient phosphorylation of serine 118 and serine 167 The increase in expression of pser118ERα was 355 ± 98 mean ± SD and of pser167ERα was 632 ± 355 These effects were enhanced in Her2 overexpressing MCF7 cells ERα expression declined to 63 ± 20 within the first 90 min of treatment and was below 10 24 h later ROS induced phosphorylation of ERα resulted in decreased expression of pS2 and progesterone receptor Activation of Erk1/2 and Akt was transient with highest levels of Erk1/2 being 595 ± 143 and pAkt 311 ± 125 Inhibition of Erk1/2 by U0126 10 μM decreased pser118ERα by 517 ± 85 and decreased pser167ERα by 419 ± 169 whereas inhibition of Akt by LY294002 20 μM and wortmannin 500 nM or by siRNA knockdown had no effect on pser167ERα expression Our data show for the first time that ROS can induce posttranslational modifications of ERα at serine 118 and serine 167 and may lead to ERα downregulation in human breast cancer cells Both the phosphorylation and consequent downregulation of ERα may be a mechanism associated with development of endocrine therapy resistanceGEW is funded by a postdoctoral fellowship from the Manitoba Health Research Council MHRC and previously from the Innovative Technologies in Multidisciplinary Health Research Training program of Canadian Institutes of Health Research CIHR WW is funded by a postdoctoral fellowship from the CancerCare Manitoba Foundation CCMF The research is supported by funding from the Canadian Institutes of Health Research CIHR and the Canadian Breast Cancer Foundation CBCF Prairies/NWT Chapter We acknowledge the strong support of the CCMF for our facilities at MICB

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