scholarly journals Sphingosine-1-Phosphate Regulates the Expression of Adherens Junction Protein E-Cadherin and Enhances Intestinal Epithelial Cell Barrier Function

2010 ◽  
Vol 56 (5) ◽  
pp. 1342-1353 ◽  
Author(s):  
Jose Greenspon ◽  
Ruiyun Li ◽  
Lan Xiao ◽  
Jaladanki N. Rao ◽  
Rex Sun ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Barrier Function ◽  
Intestinal Epithelial Cell ◽  
Adherens Junction ◽  
Intestinal Epithelial ◽  
Adherens Junction Protein ◽  
Junction Protein ◽  
Sphingosine 1 Phosphate ◽  
E Cadherin

M1760 Sphingosine-1-Phosphate Promotes Paracellular Junctional Protein Expression and Intestinal Epithelial Cell Barrier Function

2009 ◽  
Vol 136 (5) ◽  
pp. A-906
Author(s):  
Ruiyun Li ◽  
Jose Greenspon ◽  
Rao N. Jaladanki ◽  
Jian-Ying Wang ◽  
Douglas J. Turner
Keyword(s):  
Epithelial Cell ◽  
Protein Expression ◽  
Barrier Function ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Sphingosine 1 Phosphate ◽  
Junctional Protein

T1950 Sphingosine-1-Phosphate Represses Intestinal Epithelial Cell Apoptosis Through Inducing Stress Granule Formation

2010 ◽  
Vol 138 (5) ◽  
pp. S-893
Author(s):  
Ruiyun Li ◽  
Tongtong Zou ◽  
Rao N. Jaladanki ◽  
Eric D. Strauch ◽  
Jian-Ying Wang ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Apoptosis ◽  
Intestinal Epithelial Cell ◽  
Stress Granule ◽  
Intestinal Epithelial ◽  
Granule Formation ◽  
Epithelial Cell Apoptosis ◽  
Sphingosine 1 Phosphate

scholarly journals Translocation of verotoxin-1 across T84 monolayers: mechanism of bacterial toxin penetration of epithelium

1997 ◽  
Vol 273 (6) ◽  
pp. G1349-G1358 ◽  
Author(s):  
Dana J. Philpott ◽  
Cameron A. Ackerley ◽  
Amanda J. Kiliaan ◽  
Mohamed A. Karmali ◽  
Mary H. Perdue ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Barrier Function ◽  
Pathogenic Bacteria ◽  
Intestinal Epithelial Cell ◽  
Cell Function ◽  
Bacterial Toxin ◽  
General Mechanism ◽  
Epithelial Cell Line ◽  
Intestinal Epithelial ◽  
T84 Cells

Verotoxin-producing Escherichia coli (VTEC) are pathogenic bacteria associated with diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome. Verotoxins (VTs) elaborated by these organisms produce cytopathic effects on a restricted number of cell types, including endothelial cells lining the microvasculature of the bowel and the kidney. Because human intestinal epithelial cells lack the globotriaosylceramide receptor for VT binding, it is unclear how the toxin moves across the intestinal mucosa to the systemic circulation. The aims of this study were to determine the effects of VT-1 on intestinal epithelial cell function and to characterize VT-1 translocation across monolayers of T84 cells, an intestinal epithelial cell line. VT-1 at concentrations up to 1 μg/ml had no effect on the barrier function of T84 monolayers as assessed by measuring transmonolayer electrical resistance (102 ± 8% of control monolayers). In contrast, both VT-positive and VT-negative VTEC bacterial strains lowered T84 transmonolayer resistance (45 ± 7 and 38 ± 6% of controls, respectively). Comparable amounts of toxin moved across monolayers of T84 cells, exhibiting high-resistance values, as monolayers with VTEC-induced decreases in barrier function, suggesting a transcellular mode of transport. Translocation of VT-1 across T84 monolayers paralleled the movement of a comparably sized protein, horseradish peroxidase. Immunoelectron microscopy confirmed transcellular transport of VT-1, since the toxin was observed within endosomes and associated with specific intracellular targets, including the Golgi network and endoplasmic reticulum. These data present a mode of VT-1 uptake by toxin-insensitive cells and suggest a general mechanism by which bacterial toxins lacking specific intestinal receptors can penetrate the intestinal epithelial barrier.

scholarly journals The PTEN Phosphatase Controls Intestinal Epithelial Cell Polarity and Barrier Function: Role in Colorectal Cancer Progression

PLoS ONE ◽  
2010 ◽  
Vol 5 (12) ◽  
pp. e15742 ◽  
Author(s):  
Marie-Josée Langlois ◽  
Sébastien Bergeron ◽  
Gérald Bernatchez ◽  
François Boudreau ◽  
Caroline Saucier ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Epithelial Cell ◽  
Cell Polarity ◽  
Cancer Progression ◽  
Barrier Function ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Epithelial Cell Polarity ◽  
Colorectal Cancer Progression

scholarly journals PLEKHA7, an apical adherens junction protein, suppresses inflammatory breast cancer in the context of high E-cadherin and p120-catenin expression.

2020 ◽  
Author(s):  
Lindy J Pence ◽  
Antonis Kourtidis ◽  
Ryan W. Feathers ◽  
Mary T. Haddad ◽  
Sotiris Sotiriou ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Line ◽  
Inflammatory Breast Cancer ◽  
Adherens Junction ◽  
Major Protein ◽  
Breast Cancers ◽  
Adherens Junction Protein ◽  
Junction Protein ◽  
E Cadherin

Abstract Background: Inflammatory breast cancer is a highly aggressive form of breast cancer that robustly forms clusters of tumor emboli in dermal lymphatics and readily metastasizes. Inflammatory breast cancers express high levels of E-cadherin, the major protein of adherens junctions, which may enhance the ability of tumor cells to form such clusters and contribute to metastasis. Seemingly contradictory, E-cadherin has both tumor-suppressing and tumor-promoting roles in cancer; previous studies suggest that this depends on the balance between apical and basolateral cadherin-catenin complexes. Methods: In the present study, we use immunohistochemistry of inflammatory breast cancer patient samples and biochemical analysis of cell lines to determine the expression of PLEKHA7, an apical adherens junction protein. We use viral transduction to ectopically express PLEKHA7 in the SUM149 inflammatory breast cancer cell line. The effect of PLEKHA7 on the aggressiveness of inflammatory breast cancer in 2D, 3D and in-vivo were examined. Results: We determined that PLEKHA7 was deregulated in inflammatory breast cancer, demonstrating improper localization or lost expression in a strong majority of patient samples and very low expression in cell line models. We found that re-expressing PLEKHA7 is sufficient to suppress proliferation, anchorage independent growth, spheroid viability, and tumor growth in-vivo. We also observed a negative-selection pressure within the xenograft tumors to lose PLEKHA7 function or expression.Conclusions: The data indicate that PLEKHA7 is frequently deregulated and acts as a suppressor of inflammatory breast cancer. They also suggest that the resulting imbalance between apical and basolateral cadherin-catenin complexes contributes to growth, survival and emboli-forming capacities of inflammatory breast cancer.

scholarly journals Bacteroides fragilis toxin stimulates intestinal epithelial cell shedding and  -secretase-dependent E-cadherin cleavage

2007 ◽  
Vol 120 (20) ◽  
pp. 3713-3713
Author(s):  
S. Wu ◽  
K.-J. Rhee ◽  
M. Zhang ◽  
A. Franco ◽  
C. L. Sears
Keyword(s):  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Bacteroides Fragilis ◽  
Intestinal Epithelial ◽  
Cell Shedding ◽  
E Cadherin
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