Objectives: Recent studies propose the role of gonadotropins in the development and growth of endometrial carcinoma. The present research was undertaken to establish the expression of human chorionic gonadotropin (hCG), gonadotropin-releasing hormones 1 (GnRH1 and GnRH2, respectively) and their receptors in endometrial hyperplasias and carcinoma.

Material and Methods: The expression of analyzed genes in endometrial carcinoma and hyperplasia with and without atypia was evaluated using reverse transcriptase polymerase chain reaction and immunohistochemistry.

Results: The results of the experiments demonstrated the presence of hCG and GnRH1 at both messenger RNA and protein levels in endometrial carcinoma and atypical hyperplasia. Noncancerous tissue and hyperplasia without atypia demonstrated the lack of these gene coexpressions. The expression of GnRH2, LH/hCGR, and GnRHRs was heterogeneous, and the study molecules were found only in part of the analyzed tissues. The presence of hCG and GnRH1 and their receptors in cancer tissue and atypical hyperplasia suggests autocrine/paracrine action of hormones regulating the endometrial carcinoma cell proliferation.

Conclusions: The interaction between the hCG and LH/hCGR in endometrial tissue might stimulate cell growth and promote neoangiogenesis, whereas GnRHs, by binding to their receptors, could be responsible for the antiproliferative effect and stimulation of apoptosis. The identification of differences in the expression profile of the analyzed genes could be relevant for better understanding of the development of endometrial carcinomas and could be useful in clinical diagnostics.