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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

Oncogenic cooperation between H-Twist and N-Myc overrides failsafe programs in cancer cells

TL;DR: It is demonstrated that human Twist is constantly overexpressed in N-Myc-amplified neuroblastomas, and H-Twist overexpression is responsible for the inhibition of the ARF/p53 pathway involved in the Myc-dependent apoptotic response.
Journal ArticleDOI

Snail silencing effectively suppresses tumour growth and invasiveness.

TL;DR: Stable interference of endogenous Snail in two independent carcinoma cell lines leads to a dramatic reduction of in vivo tumour growth, accompanied by increased tumour differentiation and a significant decrease in the expression of MMP-9 and angiogenic markers and invasiveness, indicating that use of RNA interference can be an effective tool for blocking Snail function.
Journal ArticleDOI

Stepping out of the flow: capillary extravasation in cancer metastasis

TL;DR: Leukocyte extravasation during the inflammatory response has provided a model for transendothelial migration (TEM) of cancer cells and some progress has been made in understanding the specific roles of the Rho GTPase family, though much is still unknown.
Journal ArticleDOI

The E-cadherin gene is silenced by CpG methylation in human hepatocellular carcinomas

TL;DR: CpG methylation around the promoter region, which increases during the progression from a precancerous condition to HCC, may participate in hepatocarcinogenesis through reduction of E‐cadherin expression, resulting in loss of intercellular adhesiveness and destruction of tissue morphology.
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