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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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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.
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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

Twist2 contributes to breast cancer progression by promoting an epithelial-mesenchymal transition and cancer stem-like cell self-renewal.

TL;DR: The overexpression of Twist2 may contribute to breast cancer progression by activating the EMT programme and enhancing the self-renewal of cancer stem-like cells.
Journal ArticleDOI

EMT inducers catalyze malignant transformation of mammary epithelial cells and drive tumorigenesis towards claudin-low tumors in transgenic mice.

TL;DR: It is shown that down-regulating crucial tumor suppressor functions, EMT inducers make cells particularly prone to malignant conversion, and that cooperation between an EMT inducer and an active form of RAS is sufficient to trigger transformation of mammary epithelial cells into malignant cells.
Journal ArticleDOI

E‐cadherin and α‐, β‐, and γ‐catenin protein expression in relation to metastasis in human breast carcinoma

TL;DR: If one of these proteins is down‐regulated, the function of the others in suppressing metastasis is altered, and a significant association was seen between reduction in immunoreactivity of at least one ofThese four proteins and the presence of metastases.
Journal ArticleDOI

miR-200b mediates post-transcriptional repression of ZFHX1B

TL;DR: It is shown that Zfhx1b and miR-200b are regionally coexpressed in the adult mouse brain and that miR's activity regulates the activity of the E-cadherin promoter.
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