Literature DB >> 22863788

A comparison of epithelial-to-mesenchymal transition and re-epithelialization.

Philip L Leopold1, Jan Vincent, Hongjun Wang.   

Abstract

Wound healing and cancer metastasis share a common starting point, namely, a change in the phenotype of some cells from stationary to motile. The term, epithelial-to-mesenchymal transition (EMT) describes the changes in molecular biology and cellular physiology that allow a cell to transition from a sedentary cell to a motile cell, a process that is relevant not only for cancer and regeneration, but also for normal development of multicellular organisms. The present review compares the similarities and differences in cellular response at the molecular level as tumor cells enter EMT or as keratinocytes begin the process of re-epithelialization of a wound. Looking toward clinical interventions that might modulate these processes, the mechanisms and outcomes of current and potential therapies are reviewed for both anti-cancer and pro-wound healing treatments related to the pathways that are central to EMT. Taken together, the comparison of re-epithelialization and tumor EMT serves as a starting point for the development of therapies that can selectively modulate different forms of EMT.
Copyright © 2012 Elsevier Ltd. All rights reserved.

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Year:  2012        PMID: 22863788      PMCID: PMC3595494          DOI: 10.1016/j.semcancer.2012.07.003

Source DB:  PubMed          Journal:  Semin Cancer Biol        ISSN: 1044-579X            Impact factor:   15.707


  290 in total

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2.  A matched cohort study of the risk of cancer in users of becaplermin.

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Journal:  J Cell Biochem       Date:  2011-01       Impact factor: 4.429

Review 4.  MicroRNAs and metastasis: little RNAs go a long way.

Authors:  Derek M Dykxhoorn
Journal:  Cancer Res       Date:  2010-07-27       Impact factor: 12.701

5.  Regulation of cytokine receptors by Golgi N-glycan processing and endocytosis.

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7.  miR-200 regulates PDGF-D-mediated epithelial-mesenchymal transition, adhesion, and invasion of prostate cancer cells.

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Authors:  Barbara A Frederick; Barbara A Helfrich; Christopher D Coldren; Di Zheng; Dan Chan; Paul A Bunn; David Raben
Journal:  Mol Cancer Ther       Date:  2007-05-31       Impact factor: 6.261

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10.  Expression of N-cadherin by human squamous carcinoma cells induces a scattered fibroblastic phenotype with disrupted cell-cell adhesion.

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  31 in total

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2.  Heterogeneous Stromal Signaling within the Tumor Microenvironment Controls the Metastasis of Pancreatic Cancer.

Authors:  Agnieszka A Rucki; Kelly Foley; Pingbo Zhang; Qian Xiao; Jennifer Kleponis; Annie A Wu; Rajni Sharma; Guanglan Mo; Angen Liu; Jennifer Van Eyk; Elizabeth M Jaffee; Lei Zheng
Journal:  Cancer Res       Date:  2016-11-07       Impact factor: 12.701

Review 3.  Molecular mechanisms and treatment of radiation-induced lung fibrosis.

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4.  Rapid creation of skin substitutes from human skin cells and biomimetic nanofibers for acute full-thickness wound repair.

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Review 5.  Epigenetic control of skin and hair regeneration after wounding.

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6.  Novel naphthochalcone derivative accelerate dermal wound healing through induction of epithelial-mesenchymal transition of keratinocyte.

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7.  Epithelial Mesenchymal Transition: a double-edged sword.

Authors:  Guislaine Barriere; Pietro Fici; Giulia Gallerani; Francesco Fabbri; Michel Rigaud
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8.  The transcription factor GLI1 mediates TGFβ1 driven EMT in hepatocellular carcinoma via a SNAI1-dependent mechanism.

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9.  Partially Evoked Epithelial-Mesenchymal Transition (EMT) Is Associated with Increased TGFβ Signaling within Lesional Scleroderma Skin.

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Review 10.  Implications of the Hybrid Epithelial/Mesenchymal Phenotype in Metastasis.

Authors:  Mohit Kumar Jolly; Marcelo Boareto; Bin Huang; Dongya Jia; Mingyang Lu; Eshel Ben-Jacob; José N Onuchic; Herbert Levine
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