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A3 Adenosine Receptor Agonist Inhibited Survival of Breast Cancer Stem Cells via GLI‐1 and ERK1/2 Pathway
Author(s) -
Jafari Seyyed Mehdi,
Panjehpour Mojtaba,
Aghaei Mahmoud,
Joshaghani Hamid Reza,
Enderami Seyed Ehsan
Publication year - 2017
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.25945
Subject(s) - agonist , stem cell , cancer research , apoptosis , cancer stem cell , signal transduction , cell cycle , flow cytometry , receptor , breast cancer , cancer , biology , microbiology and biotechnology , chemistry , medicine , biochemistry
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.