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Review
. 2010 Dec;26(4):245-52.
doi: 10.5487/TR.2010.26.4.245.

Epithelial-mesenchymal Transition and Cell Invasion

Hwajin Son  1 , Aree Moon
Affiliations
Review

Epithelial-mesenchymal Transition and Cell Invasion

Hwajin Son et al. Toxicol Res. 2010 Dec.

Abstract

Epithelial-mesenchymal transition (EMT) is a complex process in which epithelial cells acquire the characteristics of invasive mesenchymal cells. EMT has been implicated in cancer progression and metastasis as well as the formation of many tissues and organs during development. Epithelial cells undergoing EMT lose cell-cell adhesion structures and polarity, and rearrange their cytoskeletons. Several oncogenic pathways such as transforming growth factor (TGF) -β, Wnt, and Notch signaling pathways, have been shown to induce EMT. These pathways have activated transcription factors including Snail, Slug, and the ZEB family which work as transcriptional repressors of E-cadherin, thereby making epithelial cells motile and resistant to apoptosis. Mounting evidence shows that EMT is associated with cell invasion and tumor progression.In this review, we summarize the characteristic features of EMT, pathways leading to EMT, and the role of EMT in cell invasion. Three topics are addressed in this review: (1) Definition of EMT, (2) Signaling pathways leading to EMT, (3) Role of EMT in cell invasion. Understanding the role of EMT in cell invasion will provide valuable information for establishing strategies to develop anti-metastatic therapeutics which modulate malignant cellular processes mediated by EMT.

Keywords: EMT; Notch; TGF-β; Wnt; cell invasion.

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References

    1. Adam L. Zhong M. Choi W. Qi W. Nicoloso M. Arora A. Calin G. Wang H. Siefker-Radtke A. McConkey D. Bar-Eli M. Dinney C. miR-200 expression regulates epithelial-to-mesenchymal transition in bladder cancer cells and reverses resistance to epidermal growth factor receptor therapy. Clin. Cancer Res. 2009;15:5060–5072. doi: 10.1158/1078-0432.CCR-08-2245. - DOI - PMC - PubMed
    1. Akiyoshi S. Inoue H. Hanai J. Kusanagi K. Nemoto N. Miyazono K. Kawabata M. c-Ski acts as a transcriptional co-repressor in transforming growth factor-beta signaling through interaction with smads. J. Biol. Chem. 1999;274:35269–35277. doi: 10.1074/jbc.274.49.35269. - DOI - PubMed
    1. Bakin A.V. Rinehart C. Tomlinson A.K. Arteaga C.L. p38 mitogen-activated protein kinase is required for TGFβ-mediated fibroblastic transdifferentiation and cell migration. J.Cell Sci. 2002;115:3193–3206. - PubMed
    1. Bakin A.V. Tomlinsos A.K. Bhowmick N.A. Moses H.L. Arteaga C.L. Phosphatidylinositol 3-kinase function is required for transforming growth factor-beta-mediated epithelial to mesenchymal transition and cell migration. J. Biol.Chem. 2000;275:36803–36810. doi: 10.1074/jbc.M005912200. - DOI - PubMed
    1. Balkwill F. Cancer and the chemokine network. Nat. Rev.Cancer. 2004;4:540–550. doi: 10.1038/nrc1388. - DOI - PubMed