Ahmadiankia, , January, 2017.Journal of Genes and Cells, 3(2017-Cell Therapy & Reg. Med.-I): p, 55-57 www.imaqpress.com doi: 10.15562/gnc.57 * Correspondence: 55 Email: ahmadiankia@shmu.ac.ir _________________________ www.genesandcells.com/journal Open Access Licensed as CC-BY Relationship between Expression of EMT Transcription Factor of ZEB1 and CXCR4 Chemokine Receptor Naghmeh Ahmadiankia Shahroud University of Medical Sciences, Shahroud, Iran Introduction Metastasis is the most common cause of death following cancer [1] and identification of mechanisms controlling this process is critical for cancer therapy. It has been declared that chemokine receptors have important roles in the process of cancer metastasis [2, 3]. CXCR4 is one of chemokine receptors that its critical role in cell migration and cancer metastasis has been revealed [4-6]. Moreover, it has been determined that metastasis is intimately associated with the program described EMT. During the passage through EMT, epithelial cancer cells lose their epithelial characteristics rather acquiring the behaviors of mesenchymal cells including migratory characteristics [7]. Considering the intimate correlation of EMT with tumor metastasis and also the important role of CXCR4 in cancer metastasis, we studied the correlation between expression of CXCR4 and EMT-TF of ZEB1 (Zinc finger E-box binding homeobox 1). Hopefully, the results will help ABSTRACT Metastasis is one the most leading cause of death from cancer and the chemokine receptor of CXCR4 has a critical role in cancer metastasis. Moreover, metastasis is always correlated with epithelial-mesenchymal transition (EMT). In this study, the correlation between expression of EMT-TF of ZEB1 and CXCR4 has been examined. The results revealed that in ZEB1 knocked out cells, the expression of CXCR4 decreased significantly. This indicated that ZEB1 might be one of the regulators of CXCR4 expression. Key words: CXCR4, Cancer, Metastasis, Epithelial Mesenchymal Transition RESEARCH ARTICLE Received 25 December 2016 Accepted 01 March 2017