Modulation of Epithelial Cell Adhesion in Gastrointestinal Homeostasis

Efstathiou, Jason A.; Pignatelli, Massimo

doi:10.1016/s0002-9440(10)65576-9

Cited by 38 publications

(21 citation statements)

References 80 publications

(84 reference statements)

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“…Cell-cell and cell-extracellular matrix adhesion play important roles in the maintenance of mechanical and functional integrity of colonic mucosa and in control of cell polarity, proliferation, and differentiation (66), and proteins implicated in cell adhesion are frequently targeted in colon tumorigenesis (67). Of 77 genes that encode proteins in the ''cell adhesion'' Gene Ontology category, 29 are overexpressed, and 48 are underexpressed after celecoxib treatment (Supplementary Table S13).…”

Section: Discussionmentioning

confidence: 99%

Celecoxib Treatment Alters the Gene Expression Profile of Normal Colonic Mucosa

Glebov

Rodríguez

Lynch³

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Section: Discussionmentioning

confidence: 99%

Celecoxib Treatment Alters the Gene Expression Profile of Normal Colonic Mucosa

Glebov

Rodríguez

Lynch³

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…In the intestine, epithelial cells differentiate from stem cells while migrating from the base of crypts to the villous surface, with apoptosis occurring both in the crypts and villi as part of normal homeostasis (17). In pathological situations such as inflammatory bowel disease, apoptosis of epithelial cells may contribute to epithelial cell loss and denudation leading to increased permeability and loss of fluid and electrolytes (5,25,26).…”

mentioning

confidence: 99%

Leukocyte elastase induces epithelial apoptosis: role of mitochondial permeability changes and Akt

Ginzberg

Shannon²,

Suzuki³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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During acute inflammation, neutrophil-mediated injury to epithelium may lead to disruption of epithelial function, including the induction of epithelial apoptosis. Herein, we report the effects of neutrophil transmigration and of purified leukocyte elastase on epithelial cell survival. Neutrophil transmigration induced apoptosis of epithelial cells [control monolayers: 5 ± 1 cells/25 high-power fields (HPF) vs. neutrophil-treated monolayers: 29 ± 10 cells/HPF, P < 0.05, n = 3 as determined by terminal deoxynucleotidyl transferase dUTP nick-end labeling assay] as did low concentrations (0.1 U/ml) of purified leukocyte elastase (control monolayers: 6.4 ± 2.5% apoptotic vs. elastase: 26.2 ± 2.9% apoptotic, P < 0.05, as determined by cytokeratin 18 cleavage). Treatment with elastase resulted in decreased mitochondrial membrane potential, release of cytochrome c to the cytosol, and cleavage of caspases-9 and -3 as determined by Western blot analysis, implicating altered mitochondrial membrane permeability as a primary mechanism for elastase-induced apoptosis. Additionally, incubation of epithelial cells with leukocyte elastase resulted in an early increase followed by a decrease in the phosphorylation of epithelial Akt, a serine/threonine kinase important in cell survival. Inhibition of epithelial Akt before elastase treatment potentiated epithelial cell apoptosis, suggesting that the initial activation of Akt represents a protective response by the epithelial cells to the proapoptotic effects of leukocyte elastase. Taken together, these observations suggest that epithelial cells exhibit a dual response to cellular stress imposed by leukocyte elastase with a proapoptotic response mediated via early alterations in mitochondrial membrane permeability countered by activation of the survival pathway involving Akt.

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“…Its direct binding to actin filament or to β-catenin maintains cell polarity and tissue architecture (43). In cancer cells, once the E-cadherin/ β-catenin complexes disappear, the actin network is disrupted modifying cell migration (44,45). Nuclear β-catenin will also increase expression of mesenchymal proteins (46,47).…”

Section: The Metastatic Processmentioning

confidence: 99%

Lipogenesis in cancer progression (Review)

Mounier

Bouraoui

Rassart

2014

International Journal of Oncology

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Abstract. In normal tissues, energy-providing lipids come principally from circulating lipids. However, in growing tumors, energy supply is mainly provided by lipids coming from de novo synthesis. It is not surprising to see elevated expression of several lipogenic genes in tumors from different origins. The role of lipogenic genes in the establishment of the primary tumor has been clearly established. A large number of studies demonstrate a role of fatty acid synthase in the activation of cell cycle and inhibition of apoptosis in tumor cells. Other lipogenic genes such as the acetyl CoA carboxylase (ACC) and the stearoyl CoA desaturase 1 (SCD1) are highly expressed in primary tumors and also appear to play a role in their development. However, the role of lipogenesis in the metastatic process is less clear. In the present review, we aim to present the most recent evidences for the key role of lipogenic enzymes in the metastatic process and in epithelial to mesenchymal transition.

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Modulation of Epithelial Cell Adhesion in Gastrointestinal Homeostasis

Cited by 38 publications

References 80 publications

Celecoxib Treatment Alters the Gene Expression Profile of Normal Colonic Mucosa

Celecoxib Treatment Alters the Gene Expression Profile of Normal Colonic Mucosa

Leukocyte elastase induces epithelial apoptosis: role of mitochondial permeability changes and Akt

Lipogenesis in cancer progression (Review)

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