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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


1 Medical Laboratory Research Center, Golestan University of Medical Sciences, Gorgan, Iran
2 Cellular and Molecular Research Center, Zahedan University of Medical Sciences, Zahedan; Department of Clinical Biochemistry, School of Pharmacy and Pharmaceutical Sciences, Isfahan, Iran
3 Department of Clinical Biochemistry, School of Pharmacy and Pharmaceutical Sciences; Isfahan Pharmaceutical Sciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
4 Department of Clinical Biochemistry, School of Pharmacy and Pharmaceutical Sciences; Bioinformatics Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
5 Department of Clinical Biochemistry, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran

Correspondence Address:
Mahmoud Aghaei,
Department of Clinical Biochemistry, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, P.O. Box: 81746-73461, Isfahan
Iran
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Source of Support: None, Conflict of Interest: None

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.


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    -  Joshaghani HR
    -  Jafari SM
    -  Aghaei M
    -  Panjehpour M
    -  Abedi H
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