Expression of G Protein-Coupled Estrogen Receptor (GPER) in endometrial adenocarcinoma and effect of agonist G-1 on growth of endometrial adenocarcinoma cell lines

• Published in: Geburtshilfe und Frauenheilkunde Vol. 73; no. 5
• Main Authors: Schüler, S, Lattrich, C, Treeck, O, Ortmann, O
• Format: Conference Proceeding Journal Article
• Language: English; German
• Published: 05.06.2013
• ISSN: 0016-5751; 1438-8804
• DOI: 10.1055/s-0033-1347873

Fragestellung: The G protein-coupled estrogen receptor (GPER) is involved in non-nuclear estrogen signaling and is expressed in a variety of hormone dependent cancer entities. This study was performed to further elucidate the role of this receptor in endometrial adenocarcinoma. Methodik: We first analyzed GPER expression in 88 endometrial cancer or normal endometrial tissue samples and compared it to those of nuclear steroid hormone receptors. Ergebnisse: In comparison to normal endometrium, GPER mRNA expression was found to be about 6-fold reduced, but still present in endometrial cancer. Expression of this receptor was decreased in all grading subgroups when compared to pre- or postmenopausal endometrium. GPER was found to be associated with expression of PR on the mRNA level (Spearman's rho 0.4610, p < 0.001). We then tested the effect of the GPER ligand G-1 on growth of three endometrial cancer cell lines with different GPER expression. GPER protein levels were hightest in RL95 – 2 cells, moderate in HEC-1A cells and not detectable in HEC-1B cells. The moderate expression level in HEC-1A cells was similar to average tumor tissue expression. Treatment with G-1 significantly inhibited growth of the GPER-positive cell lines RL95 – 2 and HEC-1A in a dose-dependent manner, whereas the GPER-negative line HEC-1B was not affected. Schlussfolgerung: Though GPER transcript levels were found to be reduced in endometrial cancer, our in vitro data suggest that moderate GPER expression might be sufficient to mediate growth-inhibitory effects triggered by its agonist G-1.