Changes in Gene Structure and Regulation of E-Cadherin during Epithelial Development, Differentiation, and Disease

Jankowski, Janusz; Bedford, Fiona K.; Kim, Young S.

doi:10.1016/s0079-6603(08)60281-0

Cited by 24 publications

(11 citation statements)

References 150 publications

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“…Generally, disorganization of interepithelial junctions is suggested to play a role in cellular dedifferentiation and carcinogenesis (19). Thus our results could have importance for two observations: 1) intestinal epithelial cells have an increased turnover in UC, with a marked increase in actively inflamed mucosa, whereas crypt cell proliferation is apparently normal in CD (13), and 2) development of malignancies is apparently more frequent in UC than in CD (37).…”

Section: Discussionmentioning

confidence: 57%

“…In sporadic colorectal carcinomas, loss of E-cadherin expression has been recorded and suggested as one important mechanism that determines invasive behavior (19). In colon cancer cell lines, formation of a complex including GSK-3, the tumor suppressor APC, and the signaling molecule ␤-catenin may imply that inactivation of the serine/threonine kinase GSK-3␤ as a downstream event of Wnt-1 signaling could promote tumorigenesis (32,53).…”

Section: Discussionmentioning

confidence: 99%

“…Experiments with a chimeric/ transgenic murine model indicate the important role of E-cadherin in the maintenance of the intestinal barrier, showing that dysregulation of this molecule leads to IBD (16). Jankowski and co-workers (19) have shown a strong correlation between the deregulation of two classic cadherin molecules, E-and P-cadherin, and the progression of human colitis (20). Furthermore, changes of intestinal permeability have been reported in patients with IBD (39,52).…”

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confidence: 99%

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Inflammatory bowel disease is associated with changes of enterocytic junctions

Gaßler

Rohr

Schneider³

et al. 2001

American Journal of Physiology-Gastrointestinal and Liver Physi

329

254

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Changes of the intestinal mucosal barrier are considered to play a role in the pathogenesis of inflammatory bowel disease (IBD). Our experiments were designed to identify dysregulation of epithelial junctional molecules in the IBD intestinum and to address whether altered expression of these molecules is a primary event in IBD or a phenomenon secondary to the inflammatory process. Noninflamed and inactively and actively inflamed mucosal tissues from patients with ulcerative colitis or Crohn's disease as well as tissues from control subjects were analyzed for the expression of junctional molecules by different methods. Marked downregulation of junctional proteins and their respective mRNAs was observed in actively inflamed IBD tissues. In IBD tissues with inactive inflammation, only a few junctional molecules such as E-cadherin and α-catenin were affected, whereas expression of desmosomal or tight junction-associated proteins appeared almost unchanged. In noninflamed IBD tissues, junctional protein expression was not different from that seen in normal control subjects. In IBD, downregulation of junctional molecule expression is apparently associated with the inflammatory process and does not likely represent a primary phenomenon.

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Section: Discussionmentioning

confidence: 57%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Inflammatory bowel disease is associated with changes of enterocytic junctions

Gaßler

Rohr

Schneider³

et al. 2001

American Journal of Physiology-Gastrointestinal and Liver Physi

329

254

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“…35 A dominant negative, N-cadherin mutant mouse model showed reduced intercellular adhesion and increased cell migration, the loss of cell diVerentiation and polarisation, and early apoptosis. 29 In addition to reduced -catenin membranous expression, previous studies have found an increase in cytoplasmic and nuclear staining, thought to be related to reduced binding to E-cadherin and, therefore, storage within the cytoplasm.…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical analysis of candidate gene product expression in the duodenal epithelium of children with coeliac sprue

Barshack

Goldberg²,

Chowers³

et al. 2001

Journal of Clinical Pathology

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Background-Coeliac sprue is a chronic disease, in which there is a characteristic mucosal lesion of the small intestine and impaired nutrient absorption, which improves upon the withdrawal of wheat gliadins and related grain proteins from the diet. Biopsy specimens demonstrate diffuse enteritis with pronounced atrophy or total loss of villi. There is also a long term risk of malignant disease. Aims-To compare the immunoexpression of DCC (deleted in colon cancer), p53, E-cadherin, and -catenin in the duodenal mucosa of children with coeliac disease with that seen in children with no evidence of small intestinal disease. Methods-To gain more insight into the genetic and immunohistochemical alterations of the duodenal epithelium in coeliac disease, 21 endoscopic biopsies from children with coeliac disease and 10 duodenal biopsies from children without coeliac disease were immunohistochemically evaluated for p53, DCC, E-cadherin, and -catenin. Results-DCC expression was not reduced in patients with coeliac disease compared with those without coeliac disease. p53 positive nuclear immunostaining was seen in seven of the 21 patients with coeliac disease. Positive nuclear staining was seen mainly in the deep and the lateral aspects of the crypts. All patients in the control group were negative for p53. In nine and three of the 21 patients with coeliac disease, respectively, the immunohistochemical expression of E-cadherin and -catenin was reduced. However, both E-cadherin and -catenin immunostaining in the control group was not altered.Conclusions-E-cadherin and -catenin were reduced in the duodenal epithelium of children with coeliac disease when compared with normal mucosa. p53 was overexpressed in the duodenal mucosa of patients with coeliac disease. The reduced expression of E-cadherin and -catenin and p53 overexpression may contribute to the morphological changes seen in the small intestinal mucosa in coeliac disease. (J Clin Pathol 2001;54:684-688)

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“…Colorectal glands play a pivotal role in performing the physiological function of the colorectal tissue and are also the origin of colorectal carcinomas. E-cadherin is essential for mediating the contact between neighboring epithelial cells and helps to establish cell polarity (Jankowski et al 1997;Jawhari et al 1997;Del Buono and Pignatelli 1999).…”

Section: Discussionmentioning

confidence: 99%

Differential distributions of CSE1L/CAS and E-cadherin in the polarized and non-polarized epithelial glands of neoplastic colorectal epithelium

Uen¹,

Tai

Shen

et al. 2010

J Mol Hist

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Colorectal glands are important functional organs in colorectal tissue and are also the origin of colorectal carcinomas. Epithelial cell polarization of colorectal glands is related to structural integrity and physiological functions of colorectal glands as well as colorectal carcinoma formation. The cellular apoptosis susceptibility (CSE1L/CAS) protein has been shown to induce polarity formation of human colorectal cells in cell culture. E-cadherin expression in epithelial cells is crucial for the establishment and maintenance of epithelial cell polarity. In this study we examined the distributions of CSE1L and E-cadherin in the epithelial glands of normal and neoplastic colorectal epithelium and correlated these to polarity formation in the colorectal glands. Our results showed that CSE1L was differentially stained in the epithelial glands of neoplastic colorectal epithelium, and the staining was related to gland epithelial cell polarization and E-cadherin distribution. CSE1L was associated E-cadherin in GST pull-down experiments and immunoprecipitation assays. Basolateral staining of CSE1L and E-cadherin were seen in the polarized glands of normal and neoplastic colorectal epithelium. Absence of basolateral CSE1L staining in neoplastic epithelium glands was associated with loss of gland epithelial cell polarity, and this was parallel with E-cadherin staining. The non-polarized areas in epithelium glands showed a patchy staining for CSE1L and E-cadherin. These results indicate that examination of CSE1L and E-cadherin distribution in colorectal epithelium glands may be valuable for evaluating the malignance of colorectal disease.

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Changes in Gene Structure and Regulation of E-Cadherin during Epithelial Development, Differentiation, and Disease

Cited by 24 publications

References 150 publications

Inflammatory bowel disease is associated with changes of enterocytic junctions

Inflammatory bowel disease is associated with changes of enterocytic junctions

Immunohistochemical analysis of candidate gene product expression in the duodenal epithelium of children with coeliac sprue

Differential distributions of CSE1L/CAS and E-cadherin in the polarized and non-polarized epithelial glands of neoplastic colorectal epithelium

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