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Stem Cells International
Volume 2016 (2016), Article ID 5285892, 10 pages
Review Article

Tackling Cancer Stem Cells via Inhibition of EMT Transcription Factors

1Graduate Program in Molecular and Cellular Biology, Stony Brook University, Stony Brook, NY 11790, USA
2Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY 11794, USA
3Stony Brook Cancer Center, Stony Brook University, Stony Brook, NY 11794, USA

Received 30 June 2016; Accepted 3 October 2016

Academic Editor: Robert Gourdie

Copyright © 2016 Megan Mladinich et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Cancer stem cell (CSC) has become recognized for its role in both tumorigenesis and poor patient prognosis in recent years. Traditional therapeutics are unable to effectively eliminate this group of cells from the bulk population of cancer cells, allowing CSCs to persist posttreatment and thus propagate into secondary tumors. The therapeutic potential of eliminating CSCs, to decrease tumor relapse, has created a demand for identifying mechanisms that directly target and eliminate cancer stem cells. Molecular profiling has shown that cancer cells and tumors that exhibit the CSC phenotype also express genes associated with the epithelial-to-mesenchymal transition (EMT) feature. Ample evidence has demonstrated that upregulation of master transcription factors (TFs) accounting for the EMT process such as Snail/Slug and Twist can reprogram cancer cells from differentiated to stem-like status. Despite being appealing therapeutic targets for tackling CSCs, pharmacological approaches that directly target EMT-TFs remain impossible. In this review, we will summarize recent advances in the regulation of Snail/Slug and Twist at transcriptional, translational, and posttranslational levels and discuss the clinical implication and application for EMT blockade as a promising strategy for CSC targeting.