Evidence for a role of epithelial mesenchymal transition during pathogenesis of fistulae in Crohnʼs disease

Bataille, Frauke; Rohrmeier, Christian; Bates, Richard C.; Weber, Achim; Rieder, Florian; Brenmoehl, Julia; Strauch, Ulrike; Farkas, S.; Fürst, Alois; Hofstädter, Ferdinand; Schölmerich, Jürgen; Herfarth, Hans H; Rogler, Gerhard

doi:10.1002/ibd.20590

Cited by 124 publications

(135 citation statements)

References 63 publications

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“…The occuring of EMT in humans' fibrosis tissue has also been demonstrated [26]. In patients with Crohn disease, the EMT was confirmed in the areas of fibrosis in the colon [27]. Furthermore, the EMT has been observed in lens epithelial cells contributing to capsular opacification after cataract surgery [10].…”

Section: Overview Of the Epithelial-mesenchymal Transition (Emt)mentioning

confidence: 91%

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The contribution of TGF-β in Epithelial–Mesenchymal Transition (EMT): Down-regulation of E-cadherin via snail

Yu¹,

Shen²,

Hong³

et al. 2015

neo

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TGF-β plays a central role in epithelial-mesenchymal transition (EMT), which is a highly conserved and reversible process that governs tumor development, invasion and metastasis. Through this transition, the epithelial cell acquires a migratory behavior which allows it to move away from the cell community and to integrate into the surrounding tissue. The cells lost epithelial phenotypes including the change of cell polarity and the loss of specialized cell-cell contacts, which related with the shortage of E-cadherin directly. The increasing reports indicated that TGF-β down-regulated the expression of E-cadherin through snail signaling pathway, which played an important role in the development of EMT. In this review, we summarized the contribution of TGF-β in EMT and discussed the molecular mechanism of snail signaling participating in the regulation of E-cadherin triggered by TGF-β.

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Section: Overview Of the Epithelial-mesenchymal Transition (Emt)mentioning

confidence: 91%

“…Cancer cell invasion is the first event in the development of metastasis. At the invasive edge of tumors, cancer cells secrete cytokines and proteases that promote angiogenesis, remodel the peri-tumoral extra- cellular matrix (ECM), and activate non-neoplastic stromal cells [27,28].…”

Section: Overview Of the Epithelial-mesenchymal Transition (Emt)mentioning

confidence: 99%

The contribution of TGF-β in Epithelial–Mesenchymal Transition (EMT): Down-regulation of E-cadherin via snail

Yu¹,

Shen²,

Hong³

et al. 2015

neo

View full text Add to dashboard Cite

show abstract

“…Defect signaling via p53 may be an early event in the progression of colitisinduced dysplasia to cancer (Dirisina et al, 2011). Bataille et al (2008) found the decreased expression of intestinal epithelial molecular marker such as E-cadherin, β-catenin, and increased expression of mesenchymal marker such as β-intergrin during the formation of fistulas in Crohn's disease. Meanwhile, they found β-catenin gradually transfer from cell membrane to cytoplasm and nucleus with the progression of EMT, and the translocation of β-catenin is considered to be the key molecular process in the development of Crohn's diseases.…”

Section: Roles Of Emt In the Pathogenesis Of Colorectal Cancer Promotmentioning

confidence: 99%

Epithelial-mesenchymal Transition and Its Role in the Pathogenesis of Colorectal Cancer

Zhu¹,

Gao²,

Wu³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Epithelial-to-mesenchymal transition (EMT) is a collection of events that allows the conversion of adherent epithelial cells, tightly bound to each other within an organized tissue, into independent fibroblastic cells possessing migratory properties and the ability to invade the extracellular matrix. EMT contributes to the complex architecture of the embryo by permitting the progression of embryogenesis from a simple single-cell layer epithelium to a complex three-dimensional organism composed of both epithelial and mesenchymal cells. However, in most tissues EMT is a developmentally restricted process and fully differentiated epithelia typically maintain their epithelial phenotype. Recently, elements of EMT, specially the loss of epithelial markers and the gain of mesenchymal markers, have been observed in pathological states, including epithelial cancers. Increasing evidence has confirmed its presence in human colon during colorectal carcinogenesis. In general, chronic inflammation is considered to be one of the causes of many human cancers including colorectal cancer(CRC). Accordingly, epidemiologic and clinical studies indicate that patients affected by ulcerative colitis and Crohn's disease, the two major forms of inflammatory bowel disease, have an increased risk of developing CRC. A large body of evidence supports roles for the SMAD/STAT3 signaling pathway, the NF-kB pathway, the Ras-mitogenactivated protein kinase/Snail/Slug and microRNAs in the development of colorectal cancers via epithelial-tomesenchymal transition. Thus, EMT appears to be closely involved in the pathogenesis of colorectal cancer, and analysis refered to it can yield novel targets for therapy.

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“…Using immunohistochemistry and in situ hybridization, an EMT was demonstrated with the www.intechopen.com expression of several markers of tubular phenotype transition, such as cytokeratin, vimentin, -SMA and zona occludens (ZO-1) in 133 kidney biopsies (Rastaldi, Ferrario et al 2002). Similarly, an expression pattern of EMT was found in areas of fibrosis in the colon in patients with Crohn's disease (Bataille, Rohrmeier et al 2008). …”

Section: Implications Of Emt In Fibrosismentioning

confidence: 99%

Tumor Inflammatory Microenvironment in EMT and Metastasis

Yuan¹,

Wu²,

Zhou³

2012

Tumor Microenvironment and Myelomonocytic Cells

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Evidence for a role of epithelial mesenchymal transition during pathogenesis of fistulae in Crohnʼs disease

Cited by 124 publications

References 63 publications

The contribution of TGF-β in Epithelial–Mesenchymal Transition (EMT): Down-regulation of E-cadherin via snail

The contribution of TGF-β in Epithelial–Mesenchymal Transition (EMT): Down-regulation of E-cadherin via snail

Epithelial-mesenchymal Transition and Its Role in the Pathogenesis of Colorectal Cancer

Tumor Inflammatory Microenvironment in EMT and Metastasis

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