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Genomic and Nongenomic Effects of Estrogen Signaling in Human Endometrial Cells: Involvement of the Growth Factor Receptor Signaling Downstream AKT Pathway

Department of Obstetrics and Gynecology Erasmus University Medical Center, Rotterdam, The Netherlands

Lindy A. M. Santegoets, MD

Department of Obstetrics and Gynecology Erasmus University Medical Center, Rotterdam, The Netherlands

Liesbeth C. M. Kühne, BSc

Reproduction and Development Eramus University Medical Center, Rotterdam, The Netherlands

Wilfred F. J. Van IJcken, PhD

Center for Biomics Erasmus University Medical Center, Rotterdam, The Netherlands

Bianca Boers-Sijmons, BSc

Department of Obstetrics and Gynecology Erasmus University Medical Center, Rotterdam, The Netherlands

Payman Hanifi-Moghaddam, PhD

Department of Molecular Design and Informatics, Organon NV, Oss, The Netherlands

Theo J. M. Helmerhorst, MD, PhD

Department of Obstetrics and Gynecology Erasmus University Medical Center, Rotterdam, The Netherlands

Leen J. Blok, PhD

Department of Obstetrics and Gynecology Erasmus University Medical Center, Rotterdam, The Netherlands, l.blok{at}erasmusmc.nl

Curt W. Burger, MD, PhD

Department of Obstetrics and Gynecology Erasmus University Medical Center, Rotterdam, The Netherlands

For the endometrium, estradiol and tamoxifen induce proliferation, and consequently, tamoxifen treatment of breast cancer results in a 2-fold to 7-fold increased risk for endometrial cancer. Here, the role of activation of growth factor receptor signaling in mediating the e fects of estrogen and tamoxifen is determined. Microarray analysis of ECC-1 cells treated with estradiol or tamoxifen indicate that rapid responses to treatment (1 hour) are very distinct from long-term responses (>24 hours). Furthermore, estradiol and tamoxifen are observed to induce AKT activation. Comparing long-term estrogen- and tamoxifen-regulated genes with genes regulated by insulin-like growth factor 1 and amphiregulin reveals that the late e fects of estrogen and tamoxifen signaling may partly be mediated via activation of growth factor receptor signaling pathways. It is hypothesized that both early and late e fects of estrogen and tamoxifen signaling in the endometrium are partly mediated via the activation of growth factor receptor signaling, putatively at the level of AKT activation.

Key Words: Estrogen • tamoxifen • insulin-like growth factor receptor • endothelial growth factor receptor • microarray • AKT • amphiregulin.

Reproductive Sciences, Vol. 14, No. 7, 646-654 (2007)
DOI: 10.1177/1933719107306872


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