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Background  Endometrial cancer is the most common gynecological cancer. G-protein coupled receptor 64 (GPR64) belongs to a family of adhesion GPCRs and plays an important role in male fertility. However, the function of GPR64 has not been studied in endometrial cancer. Our objective is to investigate the role of GPR64 in endometrial cancer.    Methods  We examined the levels of GPR64 in human endometrioid endometrial carcinoma by immunohistochemistry analysis. To determine a tumor suppressor role of GPR64 in endometrial cancer, we used a siRNA loss of function approach in human endometrial adenocarcinoma cell lines.    Results  GPR64 levels were remarkably lower in 10 of 21 (47.62%) of endometrial carcinoma samples compared to control. Depletion of  GPR64  by siRNA transfection revealed an increase of colony formation ability, cell proliferation, cell migration, and invasion activity in Ishikawa and HEC1A cells. The expression of  Connexin 43  ( Cx43 ), a member of the large family of gap junction proteins, was reduced through activation of AMP-activated protein kinase (AMPK) in Ishikawa cells with  GPR64 -deficicy.    Conclusions  These results suggest that GPR64 plays an important tumor suppressor role in endometrial cancer.    Electronic supplementary material  The online version of this article (10.1186/s12885-019-5998-1) contains supplementary material, which is available to authorized users.

G-protein coupled receptor 64 (GPR64) acts as a tumor suppressor in endometrial cancer