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

Jong Il Ahn1,2, Jung-Yoon Yoo3, Tae Hoon Kim4

  • 1Department of Agricultural Biotechnology, Seoul National University, Seoul, 08826, Republic of Korea.

BMC Cancer
|August 16, 2019
PubMed
Abstract

Insights

G-protein coupled receptor 64 (GPR64) is lower in endometrial cancer. Loss of GPR64 promotes cancer cell growth, migration, and invasion, suggesting it acts as a tumor suppressor.

Area of Science:

  • Gynecological Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Endometrial cancer is the most common gynecological malignancy.
  • G-protein coupled receptor 64 (GPR64), an adhesion GPCR, is crucial for male fertility but its role in endometrial cancer is unknown.
  • Investigating GPR64's function in endometrial cancer is critical.

Purpose of the Study:

  • To investigate the role of GPR64 in endometrial cancer.
  • To determine if GPR64 functions as a tumor suppressor in endometrial cancer.

Main Methods:

  • Immunohistochemistry was used to examine GPR64 levels in human endometrioid endometrial carcinoma.
  • A siRNA loss-of-function approach was employed in human endometrial adenocarcinoma cell lines (Ishikawa and HEC1A) to assess GPR64's impact.
  • Cell proliferation, colony formation, migration, and invasion assays were performed.

Main Results:

  • GPR64 expression was significantly lower in 47.62% of endometrial carcinoma samples compared to controls.
  • GPR64 depletion using siRNA led to increased colony formation, proliferation, migration, and invasion in cancer cells.
  • Downregulation of GPR64 reduced Connexin 43 (Cx43) expression via AMP-activated protein kinase (AMPK) activation in Ishikawa cells.

Conclusions:

  • GPR64 exhibits reduced expression in endometrial cancer.
  • GPR64 acts as a tumor suppressor in endometrial cancer.
  • GPR64 may influence endometrial cancer progression through Cx43 and AMPK pathways.
Keywords:
Connexin 43Endometrial cancerGPR64Tumor suppressor

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