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The basics of epithelial-mesenchymal transition

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TLDR
Processes similar to the EMTs associated with embryo implantation, embryogenesis, and organ development are appropriated and subverted by chronically inflamed tissues and neoplasias and the identification of the signaling pathways that lead to activation of EMT programs during these disease processes is providing new insights into the plasticity of cellular phenotypes.
Abstract
The origins of the mesenchymal cells participating in tissue repair and pathological processes, notably tissue fibrosis, tumor invasiveness, and metastasis, are poorly understood. However, emerging evidence suggests that epithelial-mesenchymal transitions (EMTs) represent one important source of these cells. As we discuss here, processes similar to the EMTs associated with embryo implantation, embryogenesis, and organ development are appropriated and subverted by chronically inflamed tissues and neoplasias. The identification of the signaling pathways that lead to activation of EMT programs during these disease processes is providing new insights into the plasticity of cellular phenotypes and possible therapeutic interventions.

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Immunity, Inflammation, and Cancer

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The Molecular Signatures Database Hallmark Gene Set Collection

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Molecular mechanisms of epithelial–mesenchymal transition

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Matrix Metalloproteinases: Regulators of the Tumor Microenvironment

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References
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Journal ArticleDOI

Alveolar epithelial cell mesenchymal transition develops in vivo during pulmonary fibrosis and is regulated by the extracellular matrix

TL;DR: Alveolar epithelial cells are revealed as progenitors for fibroblasts in vivo and implicate the provisional extracellular matrix as a key regulator of epithelial transdifferentiation during fibrogenesis.
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Variable β-catenin expression in colorectal cancers indicates tumor progression driven by the tumor environment

TL;DR: It is postulate that an important driving force for progression of well-differentiated colorectal carcinomas is the specific environment, initiating two transient phenotypic transition processes by modulating intracellular β-catenin distribution in tumor cells.
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Cadherin expression in carcinomas: role in the formation of cell junctions and the prevention of invasiveness.

TL;DR: In this article, permanent and transient molecular mechanisms are discussed which lead to the impairment of junction integrity of the epithelial cells and thus to the progression of carcinomas towards a more metastatic state.
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Identification and characterization of a fibroblast marker: FSP1.

TL;DR: Experiments in which the in vitro overexpression of FSP1 cDNA in tubular epithelium is accompanied by conversion to a mesenchymal phenotype are observed, as characterized by a more stellate and elongated fibroblast- like appearance, a reduction in cytokeratin, and new expression of vimentin.
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Transforming Growth Factor-β1 Mediates Epithelial to Mesenchymal Transdifferentiation through a RhoA-dependent Mechanism

TL;DR: The data suggest that TGF-beta rapidly activates RhoA-dependent signaling pathways to induce stress fiber formation and mesenchymal characteristics.
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