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. 2017 May 2;4:47. doi: 10.3389/fmed.2017.00047

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Copyright © 2017 Rivas-Ortiz, Lopez-Vidal, Arredondo-Hernandez and Castillo-Rojas.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Cellular and molecular pathogenesis of Helicobacter pylori infection in gastric carcinogenesis. The phosphorylated CagA active in the SHP-2/MAPK pathway regulates MEK/extracellular signal-regulated kinase (ERK), RAS/cMyc, and NF-κB pathways as a result of the regulation of genes such as hypoxia-inducible factor 1 subunit alpha (HIF-1α), mucins (MUCs), suppressor of cytokine signaling (SOCS), COX-2, inducible nitric oxide synthase (iNOS), BCL2, signal transducer and activator of transcription 3 (STAT3), matrix metalloproteinases (MMPs), and SNAIL producing proliferation, differentiation, cell survival, and increased migration, invasion, and metastasis of cancer cells. CagA alters the tight junctions independently of phosphorylation. Vacuolating cytotoxin (VacA) alters the permeability of the mitochondrial membrane and favors apoptosis.