Abstract

There was an error in the Funding statement. The correct statement is: This work was supported by grants from ARC (Association pour la Recherche contre le Cancer, Grant No. 3582) (http://www.arc-cancer.net), The Ligue Nationale Contre le Cancer (http://www.ligue-cancer.net). Muriel Busson was supported by FRM (Fondation pour la Recherche Medicale) (http://www.frm.org). DV was a recipient of the Ligue Nationale contre le Cancer. CB was supported by a HFSP fellowship (http://www.hfsp.org/). The K. B. lab is supported by the Agence Nationale de la Recherche (ANR, grant number 2010 JCJC 1104 01) (http://www.agence-nationale-recherche.fr ​/), the Universite Paris-Sud, the Institut National de la Sante et de la Recherche Medicale (INSERM) and the Ligue Nationale Contre le Cancer (Comite Val d'Oise), and is a member of the Laboratory of Excellence LERMIT (Laboratory of Excellence in Research on Medication and Innovative Therapeutics) supported by a grant from ANR (Investissements d´Avenir). Dr Madly Brigitte was supported by the Fondation ARC and Dr Carine Jacquard by INCA (Institut National du Cancer). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Highlights

  • The single epithelial cell layer that surrounds ovaries is currently believed to be one of the sources of preneoplastic lesions leading rise to epithelial ovarian tumors, which represent the vast majority of ovarian cancers [1]

  • Previous reports have shown that Estrogen-receptor beta (ERb) is weakly expressed in Epithelial ovarian cancer (EOC) tissues and derived cell lines compared to normal tissue [11]

  • We report here that the introduction of ERb in ovarian cancer cells displaying endogenous levels of ERa leads to a strong inhibition of in vivo growth and cell dissemination, mediated through the control of ERa expression and signaling

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Summary

Introduction

The single epithelial cell layer that surrounds ovaries is currently believed to be one of the sources of preneoplastic lesions leading rise to epithelial ovarian tumors, which represent the vast majority of ovarian cancers [1]. Epithelial ovarian cancer (EOC) is the seventh most common cancer. It remains the fourth most deadly one because it is difficult to diagnose at early stages and, to treat [2]. Ovary is the main organ of production of estrogens, which mainly impact on the growth, differentiation and function of reproductive tissues [3]. Through their mitogenic action, estrogens play roles in ovarian carcinogenesis. The ovaries of bERKO animals contain fewer large antral follicles and corpus luteum compared to wild-type littermates, which is concomitant with lower levels of estradiol produced [17] and a reduced expression of key genes involved in ovary function such as aromatase (Cyp19a1), LH receptor (Lhcgr), and prostaglandin synthase 2 (Ptgs2) [18]

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