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World J Stem Cells. Oct 26, 2013; 5(4): 188-195
Published online Oct 26, 2013. doi: 10.4252/wjsc.v5.i4.188
Epithelial-mesenchymal transition - activating transcription factors - multifunctional regulators in cancer
Minal Garg
Minal Garg, Department of Biochemistry, University of Lucknow, Lucknow, UP 226007, India
Author contributions: Garg M solely contributed to this paper.
Correspondence to: Minal Garg, PhD, Assistant Professor, Department of Biochemistry,University of Lucknow, Lucknow, UP 226007, India. minal14@yahoo.com
Telephone: +91-522-2348968
Received: May 17, 2013
Revised: July 6, 2013
Accepted: September 4, 2013
Published online: October 26, 2013
Processing time: 167 Days and 17.5 Hours
Abstract

The process of epithelial to mesenchymal transition (EMT), first noted during embryogenesis, has also been reported in tumor formation and leads to the development of metastatic growth. It is a naturally occurring process that drives the transformation of adhesive, non-mobile epithelial like cells into mobile cells with a mesenchymal phenotype that have ability to migrate to distant anatomical sites. Activating complex network of embryonic signaling pathways, including Wnt, Notch, hedgehog and transforming growth factor-β pathways, lead to the upregulation of EMT activating transcription factors, crucial for normal tissue development and maintenance. However, deregulation of tightly regulated pathways affecting the process of EMT has been recently investigated in various human cancers. Given the critical role of EMT in metastatic tumor formation, better understanding of the mechanistic regulation provides new opportunities for the development of potential therapeutic targets of clinical importance.

Keywords: Epithelial-to-mesenchymal transition, Metastatic growth, Embryonic signaling pathways, Transcription factors, Cancer

Core tip: This review article discusses the mechanistic regulation of embryonic signaling pathways with a special focus on epithelial mesenchymal transition (EMT)-activating transcription factors in cancer progression via modulating the process of EMT. Deciphering this mechanism may lead to the design of cancer therapies by altering the balance between the process of EMT/mesenchymal epithelial transition in cancer stem cells and thereby clinically treat the cancer.