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Copyright ©The Author(s) 2018. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastrointest Oncol. Sep 15, 2018; 10(9): 231-243
Published online Sep 15, 2018. doi: 10.4251/wjgo.v10.i9.231
Priming the seed: Helicobacter pylori alters epithelial cell invasiveness in early gastric carcinogenesis
Silvia Molina-Castro, Vanessa Ramírez-Mayorga, Warner Alpízar-Alpízar
Silvia Molina-Castro, Vanessa Ramírez-Mayorga, Cancer Epidemiology Research Program, Health Research Institute, University of Costa Rica, San José 2060, Costa Rica
Silvia Molina-Castro, Clinical Department, School of Medicine, University of Costa Rica, San José 2060, Costa Rica
Vanessa Ramírez-Mayorga, Public Nutrition Section, School of Nutrition, University of Costa Rica, San José 2060, Costa Rica
Warner Alpízar-Alpízar, Center for Research in Microscopic Structures, University of Costa Rica, San José 2060, Costa Rica
Warner Alpízar-Alpízar, Department of Biochemistry, School of Medicine, University of Costa Rica, San José 2060, Costa Rica
Author contributions: Molina-Castro S and Alpízar-Alpízar W wrote the manuscript; Ramírez-Mayorga V contributed to critical revision of the manuscript; All authors approved the final version of the article.
Supported by Vicerrectoría de Investigación of the University of Costa Rica, No. B6A11, No. B7281 and No. 90912.
Conflict-of-interest statement: There are no conflicts of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Warner Alpízar-Alpízar, PhD, Professor, Centro de Investigación en Estructuras Microscópicas, Universidad de Costa Rica, San José 2060, Costa Rica. warner.alpizar@ucr.ac.cr
Telephone: +506-25112345
Received: March 27, 2018
Peer-review started: March 27, 2018
First decision: April 10, 2018
Revised: June 13, 2018
Accepted: June 27, 2018
Article in press: June 27, 2018
Published online: September 15, 2018
Processing time: 172 Days and 8.2 Hours
Abstract

Helicobacter pylori (H. pylori) infection is a well-established risk factor for the development of gastric cancer (GC), one of the most common and deadliest neoplasms worldwide. H. pylori infection induces chronic inflammation in the gastric mucosa that, in the absence of treatment, may progress through a series of steps to GC. GC is only one of several clinical outcomes associated with this bacterial infection, which may be at least partially attributed to the high genetic variability of H. pylori. The biological mechanisms underlying how and under what circumstances H. pylori alters normal physiological processes remain enigmatic. A key aspect of carcinogenesis is the acquisition of traits that equip preneoplastic cells with the ability to invade. Accumulating evidence implicates H. pylori in the manipulation of cellular and molecular programs that are crucial for conferring cells with invasive capabilities. We present here an overview of the main findings about the involvement of H. pylori in the acquisition of cell invasive behavior, specifically focusing on the epithelial-to-mesenchymal transition, changes in cell polarity, and deregulation of molecules that control extracellular matrix remodeling.

Keywords: Helicobacter pylori; Plasminogen activation system; Invasion; Epithelial-to-mesenchymal transition; Cell polarity; Gastric carcinogenesis

Core tip:Helicobacter pylori (H. pylori) infection induces chronic inflammation in the gastric mucosa that, in the absence of treatment, may progress through a series of steps to gastric cancer (GC). GC is only one of several clinical outcomes associated with this bacterial infection, which may be at least partially attributed to the high genetic variability of H. pylori. Accumulating evidence implicates H. pylori in the manipulation of cellular and molecular programs that are crucial for conferring the cells with invasive capabilities, including reprograming of the epithelial-to-mesenchymal transition signaling programs, changing of the cell apicobasal polarity, and remodeling of the extracellular matrix.