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Mol. Hum. Reprod. Advance Access originally published online on January 4, 2008
Molecular Human Reproduction 2008 14(1):17-22; doi:10.1093/molehr/gam081
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© The Author 2008. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Glycodelin blocks progression to S phase and inhibits cell growth: a possible progesterone-induced regulator for endometrial epithelial cell growth

Kuniaki Ohta1,2, Tetsuo Maruyama1,3, Hiroshi Uchida1, Masanori Ono1, Takashi Nagashima1, Toru Arase1, Takashi Kajitani1, Hideyuki Oda1, Mineto Morita2 and Yasunori Yoshimura1

1Department of Obstetrics and Gynecology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku, Tokyo 160-8582, Japan 2Department of Obstetrics and Gynecology, Toho University School of Medicine, Tokyo 143-8541, Japan

3 Correspondence address. E-mail: tetsuo{at}sc.itc.keio.ac.jp

Prolonged exposure to unopposed estrogen in the absence of progesterone gives rise to endometrial hyperplasia and carcinoma. Post-ovulatory progesterone is necessary for the proper growth and differentiation of endometrial epithelial cells (EECs). Progesterone exposure induces the endometrial production of numerous bioactive substances, one of which is the glycoprotein, glycodelin (Gd). We investigated the role of Gd in cell cycle progression and cell growth to better understand how Gd affects EEC behavior and endometrial cancer pathogenesis. Ishikawa cells, a well-differentiated human endometrial epithelial cancer cell line, were transfected with expression plasmids encoding enhanced green fluorescent protein (EGFP) or EGFP-fused Gd (EGFP-Gd). They were then subjected to a cell proliferation assay, flow cytometry cell cycle analysis and RT–PCR analysis of cyclin-dependent kinase inhibitors (CDKIs) including p21, p27 and p16. Overexpression of EGFP-Gd resulted in a reduction of cell proliferation activity, an accumulation of G1-phase cells and up-regulation of p21, p27 and p16 mRNAs. Furthermore, progesterone-induced inhibition of Ishikawa cell growth was partially attenuated by Gd knockdown using siRNA. These results indicate that Gd causes inhibition of G1/S progression together with up-regulation of CDKIs thereby reducing cell growth. Thus, progesterone-induced expression of Gd may, at least in part, contribute to the suppression of endometrial epithelial growth observed during the secretory phase.

Key words: glycodelin/endometrium/cell cycle/cyclin-dependent kinase inhibitors/progesterone

Submitted on September 2, 2007; resubmitted on November 4, 2007; accepted on November 26, 2007.


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