G-Protein-coupled estrogen receptor (GPER)-specific agonist G-1 reduces cell proliferation in gastrointestinal cancer cells independently of GPER1 receptor presence
DOI:
https://doi.org/10.56782/pps.743Keywords:
AGS cells, colon cancer, estrogen receptors, gastric cancer, HT-29 cellsAbstract
Cancer is considered the second leading cause of death worldwide, following cardiovascular diseases. It is believed that the effect of estrogen is not only limited to tumors of hormonally regulated tissues such as the breast, endometrium, and ovary, but also plays a role in the development of gastric and colorectal cancer. Therefore, this study aimed to investigate the apoptotic and antiproliferative effects of G-Protein-Coupled Estrogen Receptor (GPER)-Specific Agonist G-1 on gastrointestinal adenocarcinoma cells. G-1 was applied to human gastric cancer (AGS) and human colon cancer (HT-29) cells at different concentrations. Real-time cellular analysis (RTCA) and MTT assay were used to evaluate cell proliferation. Flow cytometry was employed for the detection of early and late apoptosis using the Annexin-V FITC Kit, Hoechst staining, and analysis of Caspase-3 activation. siRNA was used to knockdown GPER1 expression at the transcriptional level. G-1 exhibited concentration- and time-dependent antiproliferative effects on AGS and HT-29 cells. At the highest concentration, G-1 induced apoptosis in both cell lines. G-1 showed similar antiproliferative effects on cells with and without siRNA treatment. The data suggest that the antiproliferative effects of G-1 appeared to be independent of GPER1 activation G-1 appears to be an attractive tool for suggesting novel targets in the treatment of gastric and colorectal adenocarcinomas.
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