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Mitochondrial and Caspase Pathways Are Involved in the Induction of Apoptosis by Ib-Meca in Ovarian Cancer Cell Lines Publisher Pubmed



Abedi H1 ; Aghaei M1 ; Panjehpour M1, 2 ; Hajiahmadi S1
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Authors Affiliations
  1. 1. Department of Clinical Biochemistry, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, P.O. Box: 81746-73461, Isfahan, Iran
  2. 2. Bioinformatics Research Center, Isfahan University of Medical Sciences, Isfahan, Iran

Source: Tumor Biology Published:2014


Abstract

A3 adenosine receptor agonist (IB-MECA) has been shown to play important roles in cell proliferation and apoptosis in a variety of cancer cell lines. The present study was designed to understand the mechanism underlying IB-MECA-induced apoptosis in human ovarian cancer cell lines. The messenger RNA (mRNA) and protein expression levels of A3 adenosine receptor were detected in OVCAR-3 and Caov-4 ovarian cancer cells. IB-MECA was capable of decreasing intracellular cyclic adenosine monophosphate (cAMP) that was the reason for the presence of functional A3 adenosine receptor on the cell lines. IB-MECA significantly reduced cell viability in a dose-dependent manner. Cytotoxicity of IB-MECA was suppressed by MRS1220, an A3 adenosine receptor antagonist. The growth inhibition effect of IB-MECA was related to the induction of cell apoptosis, which was manifested by annexin V-FITC staining, activation of caspase-3 and caspase-9, and loss of mitochondrial membrane potentials (ΔΨm). In addition, downregulation of the regulatory protein Bcl-2 and upregulation of Bax protein by IB-MECA were also observed. These findings demonstrated that IB-MECA induces apoptosis via the mitochondrial signaling pathway. These suggest that A3 adenosine receptor agonists may be a potential agent for induction of apoptosis in human ovarian cancer cells. © 2014, International Society of Oncology and BioMarkers (ISOBM).
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