Abstract
BackgroundEndometrial 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.MethodsWe 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.ResultsGPR64 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.ConclusionsThese results suggest that GPR64 plays an important tumor suppressor role in endometrial cancer.
Highlights
Endometrial cancer is the most common gynecological cancer
The levels of G-protein coupled receptor 64 (GPR64) were significantly lower in 47.62% (10/21) of endometrial cancer tissue compared with controls (p < 0.001)
These results suggest that GPR64 may play a tumor suppressor role in certain cases of endometrial cancer
Summary
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. Endometrial cancer is the most common gynecologic malignancy, with an estimated 63,230 new cases in 2018 [1]. The most common type of endometrial cancer is endometrioid adenocarcinoma, which originates from endometrial epithelial cells [2]. The development of endometrial hyperplasia, a proliferative process in the epithelium, is the abnormal thickening of the lining of the uterus due to an increase in the number of endometrial glands. It is a critical risk factor for endometrioid endometrial carcinoma [3]. Loss of GPR64 in ewing sarcoma cell line leads to decreased PGF and MMP1 expression and reduced
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