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A3 Adenosine Receptor Agonist Inhibited Survival of Breast Cancer Stem Cells Via Gli-1 and Erk1/2 Pathway Publisher Pubmed



Jafari SM1 ; Panjehpour M1, 2 ; Aghaei M1, 3 ; Joshaghani HR4 ; Enderami SE5
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Authors Affiliations
  1. 1. Department of Clinical Biochemistry, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran
  2. 2. Bioinformatics Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
  3. 3. Isfahan Pharmaceutical Sciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
  4. 4. Medical Laboratory Research Center, Golestan University of Medical Sciences, Gorgan, Iran
  5. 5. Faculty of Medicine, Department of Medical Biotechnology and Nanotechnology, Zanjan University of Medical Sciences, Zanjan, Iran

Source: Journal of Cellular Biochemistry Published:2017


Abstract

Numerous studies have demonstrated the role of A3 adenosine receptor (A3AR) and signaling pathways in the multiple aspects of the tumor. However, there is a little study about the function of A3AR in the biological processes of cancer stem cells (CSCs). CSCs have a critical role in the maintenance and survival of breast cancer. The aim of current study was to investigate the effect of A3AR agonist on breast cancer stem cells (BCSCs). XTT assay showed antiproliferative effect of A3AR agonist (Cl-IB-MECA) on BCSCs. Our results also demonstrated that A3AR agonist reduces mammosphere formation in a dose-dependent manner. Flow cytometry analysis showed that A3AR agonist induces G1 cell cycle arrest and apoptosis in BCSCs. Western blot assay showed that A3AR agonist inhibits the expression of cell cycle and apoptotic regulatory proteins as well as the expression of ERK1/2 and GLI-1 proteins. Finally, these findings propose that A3AR agonist induces cell cycle arrest and apoptosis in BCSCs by inhibition of ERK1/2 and GLI-1 cascade. J. Cell. Biochem. 118: 2909–2920, 2017. © 2017 Wiley Periodicals, Inc. © 2017 Wiley Periodicals, Inc.
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