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A3 Adenosine Receptor Agonist Induce G1 Cell Cycle Arrest Via Cyclin D and Cyclin-Dependent Kinase 4 Pathways in Ovcar-3 and Caov-4 Cell Lines Publisher Pubmed



Joshaghani H1 ; Jafari S2, 3 ; Aghaei M3, 4 ; Panjehpour M3, 5 ; Abedi H3
Authors

Source: Journal of Cancer Research and Therapeutics Published:2017


Abstract

Aim of the Study: The cell cycle, a vital process that involves in cells' growth and division, lies at the heart of cancer. It has been shown that IB-MECA, an A3 adenosine receptor agonist inhibits the proliferation of cancer cells by inducing cell cycle arrest in several tumors. In this study, we evaluated the role of IB-MECA inhibition in cell cycle progression in ovarian cancer cells. Materials and Methods: Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay in Caov-4 and OVCAR-3. Analysis of cell cycle distribution was carried out by flow cytometry. To determine the mechanisms of IB-MECA-mediated induction of cell cycle arrest, the expression of cell cycle regulatory proteins Cyclin D1 and cyclin-dependent kinase 4 (CDK4) was evaluated. Results: Our results showed that IB-MECA significantly reduced cell viability in a dose-dependent manner. Moreover, our results indicated that a low concentration of IB-MECA induced G1 cell cycle arrest. Reduction of Cyclin D1 and CDK4 protein levels was also observed after treating cancer cells with IB-MECA. Conclusion: This study demonstrated that IB-MECA induces G1 phase cell cycle arrest through Cyclin D1/CDK4-mediated pathway in ovarian cancer cells. © 2017 Journal of Cancer Research and Therapeutics.
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Mahmoud Aghaei (13)
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