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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

Epithelial-mesenchymal transition of tubular epithelial cells in human renal biopsies.

TL;DR: The results suggest that, via transition to a mesenchymal phenotype, TEC can produce ECM proteins in human disease and directly intervene in the fibrotic processes.
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Integrin β1 Signaling Is Necessary for Transforming Growth Factor-β Activation of p38MAPK and Epithelial Plasticity

TL;DR: TGF-β-mediated p38 MAPK activation is dependent on functional integrin β1, and p38MAPK activity is required but is not sufficient to induce EMT.
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Nodal Antagonists in the Anterior Visceral Endoderm Prevent the Formation of Multiple Primitive Streaks

TL;DR: These findings provide support for a model whereby Cerberus-like and Lefty1 in the anterior visceral endoderm restrict primitive streak formation to the posterior end of mouse embryos by antagonizing Nodal signaling, and both antagonists are also required for proper patterning of the primitive streak.
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Induction of the neural crest: a multigene process.

TL;DR: This recent work has revealed that induction of the neural crest is a complex multistep process that involves many genes.
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E-cadherin regulates cell growth by modulating proliferation-dependent β-catenin transcriptional activity

TL;DR: It is concluded that β-catenin transcriptional activity is essential for cell proliferation and can be controlled by E-cadherin in a cell adhesion-independent manner.
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