G protein-coupled estrogen receptor 1 agonist G-1 induces cell cycle arrest in the mitotic phase, leading to apoptosis in endometriosis

Lab / animal OA: closed CC0 ⤵ 16 in-corpus citations
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The G protein-coupled estrogen receptor 1 agonist G-1 was found to induce cell cycle arrest in the mitotic phase, ultimately leading to apoptosis in endometriosis.

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Abstract

OBJECTIVE: To demonstrate the effects of the selective G protein-coupled estrogen receptor 1 (GPER) agonist G-1 in human ovarian endometriotic stromal cells (ESCs). DESIGN: Experimental in vitro study. SETTING: University hospital. PATIENT(S): A total of 33 patients with ovarian endometrioma. INTERVENTION(S): Endometriotic stromal cells from ovarian chocolate cysts were treated with the GPER agonist G-1. MAIN OUTCOME MEASURE(S): The primary outcomes were cell proliferation, measured using the WST-8 assay; cell cycle, as analyzed using flow cytometry, fluorescent immunocytochemistry, and cytotoxicity; caspase activity, as measured by fluorescent and luminescent enzyme assays; and protein expression levels, as determined by Western blot analysis. RESULT(S): G-1 suppressed ESC proliferation in a concentration-dependent manner. The inhibitory effect was not blocked when GPER signaling pathways, including the GPER itself, were inhibited. G-1 induced cell cycle arrest and accumulation in the sub-G1 phase in ESCs. Immunofluorescence analysis demonstrated that G-1 interrupted microtubule assembly at the mitotic phase. G-1 also induced caspase-3-dependent apoptosis without significant cytotoxicity. CONCLUSION(S): G-1 suppressed proliferation and induced apoptosis in ESCs, suggesting the potential use of this compound as a therapeutic drug for the treatment of endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Apoptosis Cell Proliferation Cyclopentanes Endometriosis M Phase Cell Cycle Checkpoints Ovarian Cysts Ovary Quinolines Receptors, G-Protein-Coupled Stromal Cells Adult Adult Apoptosis Apoptosis Caspase 3 Caspase 3 Caspase 3 Cell Proliferation Cell Proliferation Cells, Cultured

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