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Open AccessJournal ArticleDOI

Epithelial–mesenchymal plasticity in carcinoma metastasis

Jeff H. Tsai, +1 more
- 15 Oct 2013 - 
- Vol. 27, Iss: 20, pp 2192-2206
TLDR
The functional requirement of EMT and/or MET during the individual steps of tumor metastasis is reviewed and the potential of targeting this program when treating metastatic diseases is discussed.
Abstract
Tumor metastasis is a multistep process by which tumor cells disseminate from their primary site and form secondary tumors at a distant site. Metastasis occurs through a series of steps: local invasion, intravasation, transport, extravasation, and colonization. A developmental program termed epithelial-mesenchymal transition (EMT) has been shown to play a critical role in promoting metastasis in epithelium-derived carcinoma. Recent experimental and clinical studies have improved our knowledge of this dynamic program and implicated EMT and its reverse program, mesenchymal-epithelial transition (MET), in the metastatic process. Here, we review the functional requirement of EMT and/or MET during the individual steps of tumor metastasis and discuss the potential of targeting this program when treating metastatic diseases.

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Citations
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Circulating tumour cells in the -omics era: how far are we from achieving the ‘singularity’?

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Downregulation of UHRF1 promotes EMT via inducing CXCR4 in human cancer cells.

TL;DR: It is found that downregulation of U HRF1 enhances the migratory and invasive properties of human cancer cells by inducing EMT, and that the CXCR4 signaling pathway is strictly necessary for UHRF1 deficiency-mediated induction of EMT.
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Pre-metastatic niche triggers SDF-1/CXCR4 axis and promotes organ colonisation by hepatocellular circulating tumour cells via downregulation of Prrx1.

TL;DR: It is demonstrated that decreased expression of Prrx1 stimulates SDF-1/CXCR4 signalling and contributes to organ colonisation with blood CTCs in HCC.
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DSTYK Promotes Metastasis and Chemoresistance via EMT in Colorectal Cancer.

TL;DR: DSTYK is identified as a novel protein kinase in regulating TGF-β–mediated EMT and chemoresistance in CRC cells, which defines DSTyK as a potential therapeutic target for CRC therapy.
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