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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
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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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Galectin-1 induces metastasis and epithelial-mesenchymal transition (EMT) in human ovarian cancer cells via activation of the MAPK JNK/p38 signalling pathway.

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HMG20A is required for SNAI1-mediated epithelial to mesenchymal transition.

TL;DR: This work shows that HMG20A together with LSD1 are required for SNAI1-dependent repression of epithelial genes and for (transforming growth factor β) TGF-β-triggered EMT, and shows that expression of H MG20A correlates positively with mesenchymal markers and negatively with epithelial markers in human tumor samples.
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Circulating tumour cells and the epithelial mesenchymal transition in colorectal cancer

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Mesenchymal-Epithelial Transition and Circulating Tumor Cells in Small Cell Lung Cancer

TL;DR: A panel of SCLC CTC cell line from patients with relapsing disease, which share characteristic markers of this malignancy and a primarily epithelial phenotype with unique formation of large tumorospheres, containing quiescent and hypoxic cells are obtained.
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RAS, Cellular Plasticity, and Tumor Budding in Colorectal Cancer.

TL;DR: This review is focused on the current knowledge on RAS in CRC and its link with cellular plasticity and related clinicopathological features.
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