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CagA Associates with c-Met, E-Cadherin, and p120-Catenin in a Multiproteic Complex That Suppresses Helicobacter pylori-Induced Cell-Invasive Phenotype

MJ Oliveira, AM Costa, AC Costa, RM Ferreira, P Sampaio, JC Machado, R Seruca, Marc Mareel UGent and C Figueiredo (2009) JOURNAL OF INFECTIOUS DISEASES. 200(5). p.745-755
abstract
Background. Helicobacter pylori induces an invasive phenotype in gastric epithelial cells through a mechanism that requires the type IV secretion system and the phosphorylation of c-Met. The E-cadherin-catenin complex is a major component of the adherens junctions and functions as an invasion suppressor. We investigated whether E-cadherin has a role in H. pylori-induced, c-Met phosphorylation- dependent cell-invasive phenotype. Methods. AGS cells that lack E-cadherin and that are invasive to H. pylori stimulation were transduced with E-cadherin and infected with H. pylori. NCI-N87 cells, which endogenously express E-cadherin, were also used for infection experiments. Results. E-cadherin was sufficient to suppress not only H. pylori-mediated cell-invasive phenotype but also c-Met and p120-catenin tyrosine phosphorylation. H. pylori infection led to increased interactions between E-cadherin and p120-catenin, c-Met and E-cadherin, and c-Met and p120-catenin. Using in vitro infection assays, we showed that H. pylori CagA interacts with E-cadherin, p120-catenin, and c-Met. Finally, using small interfering RNA, we showed that interactions between CagA and E-cadherin and between CagA and p120-catenin were established through c-Met. Conclusions. We suggest that H. pylori alters the E-cadherin-catenin complex, leading to formation of a multiproteic complex composed of CagA, c-Met, E-cadherin, and p120-catenin. This complex abrogates c-Met and p120-catenin tyrosine phosphorylation and suppresses the cell-invasive phenotype induced by H. pylori.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (proceedingsPaper)
publication status
published
journal title
JOURNAL OF INFECTIOUS DISEASES
J. Infect. Dis.
volume
200
issue
5
pages
745 - 755
conference name
Digestive Disease Week Meeting/109th Annual Meeting of the American-Gastroenterological-Association
conference location
San Diego, CA
conference start
2008-05-17
conference end
2008-05-22
Web of Science type
Proceedings Paper
Web of Science id
000268683900013
JCR category
INFECTIOUS DISEASES
JCR impact factor
5.865 (2009)
JCR rank
4/57 (2009)
JCR quartile
1 (2009)
ISSN
0022-1899
DOI
10.1086/604727
language
English
UGent publication?
yes
classification
A1
id
849916
handle
http://hdl.handle.net/1854/LU-849916
date created
2010-02-02 16:41:49
date last changed
2010-02-16 10:59:58
@article{849916,
  abstract     = {Background. Helicobacter pylori induces an invasive phenotype in gastric epithelial cells through a mechanism that requires the type IV secretion system and the phosphorylation of c-Met. The E-cadherin-catenin complex is a major component of the adherens junctions and functions as an invasion suppressor. We investigated whether E-cadherin has a role in H. pylori-induced, c-Met phosphorylation- dependent cell-invasive phenotype.

Methods. AGS cells that lack E-cadherin and that are invasive to H. pylori stimulation were transduced with E-cadherin and infected with H. pylori. NCI-N87 cells, which endogenously express E-cadherin, were also used for infection experiments.

Results. E-cadherin was sufficient to suppress not only H. pylori-mediated cell-invasive phenotype but also c-Met and p120-catenin tyrosine phosphorylation. H. pylori infection led to increased interactions between E-cadherin and p120-catenin, c-Met and E-cadherin, and c-Met and p120-catenin. Using in vitro infection assays, we showed that H. pylori CagA interacts with E-cadherin, p120-catenin, and c-Met. Finally, using small interfering RNA, we showed that interactions between CagA and E-cadherin and between CagA and p120-catenin were established through c-Met.

Conclusions. We suggest that H. pylori alters the E-cadherin-catenin complex, leading to formation of a multiproteic complex composed of CagA, c-Met, E-cadherin, and p120-catenin. This complex abrogates c-Met and p120-catenin tyrosine phosphorylation and suppresses the cell-invasive phenotype induced by H. pylori.},
  author       = {Oliveira, MJ and Costa, AM and Costa, AC and Ferreira, RM and Sampaio, P and Machado, JC and Seruca, R and Mareel, Marc and Figueiredo, C},
  issn         = {0022-1899},
  journal      = {JOURNAL OF INFECTIOUS DISEASES},
  language     = {eng},
  location     = {San Diego, CA},
  number       = {5},
  pages        = {745--755},
  title        = {CagA Associates with c-Met, E-Cadherin, and p120-Catenin in a Multiproteic Complex That Suppresses Helicobacter pylori-Induced Cell-Invasive Phenotype},
  url          = {http://dx.doi.org/10.1086/604727},
  volume       = {200},
  year         = {2009},
}

Chicago
Oliveira, MJ, AM Costa, AC Costa, RM Ferreira, P Sampaio, JC Machado, R Seruca, Marcus Mareel, and C Figueiredo. 2009. “CagA Associates with c-Met, E-Cadherin, and p120-Catenin in a Multiproteic Complex That Suppresses Helicobacter pylori-Induced Cell-Invasive Phenotype.” Journal of Infectious Diseases 200 (5): 745–755.
APA
Oliveira, M., Costa, A., Costa, A., Ferreira, R., Sampaio, P., Machado, J., Seruca, R., et al. (2009). CagA Associates with c-Met, E-Cadherin, and p120-Catenin in a Multiproteic Complex That Suppresses Helicobacter pylori-Induced Cell-Invasive Phenotype. JOURNAL OF INFECTIOUS DISEASES, 200(5), 745–755. Presented at the Digestive Disease Week Meeting/109th Annual Meeting of the American-Gastroenterological-Association.
Vancouver
1.
Oliveira M, Costa A, Costa A, Ferreira R, Sampaio P, Machado J, et al. CagA Associates with c-Met, E-Cadherin, and p120-Catenin in a Multiproteic Complex That Suppresses Helicobacter pylori-Induced Cell-Invasive Phenotype. JOURNAL OF INFECTIOUS DISEASES. 2009;200(5):745–55.
MLA
Oliveira, MJ, AM Costa, AC Costa, et al. “CagA Associates with c-Met, E-Cadherin, and p120-Catenin in a Multiproteic Complex That Suppresses Helicobacter pylori-Induced Cell-Invasive Phenotype.” JOURNAL OF INFECTIOUS DISEASES 200.5 (2009): 745–755. Print.