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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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Journal ArticleDOI

The RNA binding protein quaking regulates formation of circRNAs.

TL;DR: It is shown that hundreds of circRNAs are regulated during human epithelial-mesenchymal transition (EMT) and that the production of over one-third of abundant circ RNAs is dynamically regulated by the alternative splicing factor, Quaking (QKI), which itself is regulated during EMT.
Journal ArticleDOI

Signaling mechanisms of the epithelial-mesenchymal transition

TL;DR: This review discusses how intracellular pathways and extracellular signals that regulate gene expression to induce EMT crosstalk and respond to signals from the microenvironment to regulate the expression and function of EMT-inducing transcription factors in development, physiology, and disease.
Journal ArticleDOI

Guidelines and definitions for research on epithelial–mesenchymal transition

Jing Yang, +47 more
TL;DR: This Consensus Statement is the outcome of a 2-year-long discussion among EMT researchers and aims to both clarify the nomenclature and provide definitions and guidelines for EMT research in future publications to reduce misunderstanding and misinterpretation of research data generated in various experimental models.
Journal ArticleDOI

The Immunomodulatory and Anti-Inflammatory Role of Polyphenols.

TL;DR: It is shown that polyphenols can play a beneficial role in the prevention and the progress of chronic diseases related to inflammation such as diabetes, obesity, neurodegeneration, cancers, and cardiovascular diseases, among other conditions.
References
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Journal ArticleDOI

Matrix metalloproteinases stimulate epithelial-mesenchymal transition during tumor development

TL;DR: An overview of recent findings of MMP action in tumors and the mechanisms by which MMPs induce both phenotypic and genotypic alterations that facilitate tumor progression is provided.
Journal ArticleDOI

Twist Modulates Breast Cancer Stem Cells by Transcriptional Regulation of CD24 Expression

TL;DR: The direct involvement of Twist in generating a breast cancer stem cell phenotype through down-regulation of CD24 expression and independent of an epithelial-mesenchymal transition is demonstrated.
Journal ArticleDOI

Multiple ways of silencing E-cadherin gene expression in lobular carcinoma of the breast.

TL;DR: It is concluded that most ILCs show genetic or epigenetic changes affecting the E‐cadherin gene and that many of these tumours lack E‐ cadher in expression, consistent with biallelic inactivation of CDH1 by promoter methylation, mutation or allelic loss in any combination.
Journal ArticleDOI

Sustained TGF beta exposure suppresses Smad and non-Smad signalling in mammary epithelial cells, leading to EMT and inhibition of growth arrest and apoptosis

TL;DR: In this article, mammary epithelial NMuMG cells were analyzed in response to short and long-term TGFbeta exposure, and both cell cycle arresting/proapoptotic and anti-proliferation and EMT-promoting signalling pathways (Smads, p38 kinase) were co-suppressed to low but significant levels.
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