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Helicobacter pylori Strains and Gastric MALT Lymphoma

Proteolysis in Helicobacter pylori-Induced Gastric Cancer

Division of Microbiology, Department of Molecular Biology, Paris-Lodron University of Salzburg, Salzburg 5020, Austria
Leeds Institute Biomedical and Clinical Sciences, St. James’s University Hospital, University of Leeds, Leeds LS9 7TF, UK
Author to whom correspondence should be addressed.
Academic Editor: Timothy L. Cover
Toxins 2017, 9(4), 134;
Received: 14 February 2017 / Revised: 3 April 2017 / Accepted: 6 April 2017 / Published: 11 April 2017
(This article belongs to the Special Issue H. pylori Virulence Factors in the Induction of Gastric Cancer)
Persistent infections with the human pathogen and class-I carcinogen Helicobacter pylori (H. pylori) are closely associated with the development of acute and chronic gastritis, ulceration, gastric adenocarcinoma and lymphoma of the mucosa-associated lymphoid tissue (MALT) system. Disruption and depolarization of the epithelium is a hallmark of H. pylori-associated disorders and requires extensive modulation of epithelial cell surface structures. Hence, the complex network of controlled proteolysis which facilitates tissue homeostasis in healthy individuals is deregulated and crucially contributes to the induction and progression of gastric cancer through processing of extracellular matrix (ECM) proteins, cell surface receptors, membrane-bound cytokines, and lateral adhesion molecules. Here, we summarize the recent reports on mechanisms how H. pylori utilizes a variety of extracellular proteases, involving the proteases Hp0169 and high temperature requirement A (HtrA) of bacterial origin, and host matrix-metalloproteinases (MMPs), a disintegrin and metalloproteinases (ADAMs) and tissue inhibitors of metalloproteinases (TIMPs). H. pylori-regulated proteases represent predictive biomarkers and attractive targets for therapeutic interventions in gastric cancer. View Full-Text
Keywords: Helicobacter pylori; protease; MMP; ADAM; TIMP; E-cadherin; HtrA; EGFR Helicobacter pylori; protease; MMP; ADAM; TIMP; E-cadherin; HtrA; EGFR
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MDPI and ACS Style

Posselt, G.; Crabtree, J.E.; Wessler, S. Proteolysis in Helicobacter pylori-Induced Gastric Cancer. Toxins 2017, 9, 134.

AMA Style

Posselt G, Crabtree JE, Wessler S. Proteolysis in Helicobacter pylori-Induced Gastric Cancer. Toxins. 2017; 9(4):134.

Chicago/Turabian Style

Posselt, Gernot, Jean E. Crabtree, and Silja Wessler. 2017. "Proteolysis in Helicobacter pylori-Induced Gastric Cancer" Toxins 9, no. 4: 134.

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