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Influence of Helicobacter pylori oncoprotein CagA in gastric cancer: A critical-reflective analysis

Gastric cancer is the fifth most common malignancy and third leading cancer-related cause of death worldwide. Helicobacter pylori is a Gram-negative bacterium that inhabits the gastric environment of 60.3% of the world’s population and represents the main risk factor for the onset of gastric neoplas...

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Autores principales: Freire de Melo, Fabrício, Marques, Hanna Santos, Rocha Pinheiro, Samuel Luca, Lemos, Fabian Fellipe Bueno, Silva Luz, Marcel, Nayara Teixeira, Kádima, Souza, Cláudio Lima, Oliveira, Márcio Vasconcelos
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Baishideng Publishing Group Inc 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9724182/
https://www.ncbi.nlm.nih.gov/pubmed/36483973
http://dx.doi.org/10.5306/wjco.v13.i11.866
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author Freire de Melo, Fabrício
Marques, Hanna Santos
Rocha Pinheiro, Samuel Luca
Lemos, Fabian Fellipe Bueno
Silva Luz, Marcel
Nayara Teixeira, Kádima
Souza, Cláudio Lima
Oliveira, Márcio Vasconcelos
author_facet Freire de Melo, Fabrício
Marques, Hanna Santos
Rocha Pinheiro, Samuel Luca
Lemos, Fabian Fellipe Bueno
Silva Luz, Marcel
Nayara Teixeira, Kádima
Souza, Cláudio Lima
Oliveira, Márcio Vasconcelos
author_sort Freire de Melo, Fabrício
collection PubMed
description Gastric cancer is the fifth most common malignancy and third leading cancer-related cause of death worldwide. Helicobacter pylori is a Gram-negative bacterium that inhabits the gastric environment of 60.3% of the world’s population and represents the main risk factor for the onset of gastric neoplasms. CagA is the most important virulence factor in H. pylori, and is a translocated oncoprotein that induces morphofunctional modifications in gastric epithelial cells and a chronic inflammatory response that increases the risk of developing precancerous lesions. Upon translocation and tyrosine phosphorylation, CagA moves to the cell membrane and acts as a pathological scaffold protein that simultaneously interacts with multiple intracellular signaling pathways, thereby disrupting cell proliferation, differentiation and apoptosis. All these alterations in cell biology increase the risk of damaged cells acquiring pro-oncogenic genetic changes. In this sense, once gastric cancer sets in, its perpetuation is independent of the presence of the oncoprotein, characterizing a “hit-and-run” carcinogenic mechanism. Therefore, this review aims to describe H. pylori- and CagA-related oncogenic mechanisms, to update readers and discuss the novelties and perspectives in this field.
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spelling pubmed-97241822022-12-07 Influence of Helicobacter pylori oncoprotein CagA in gastric cancer: A critical-reflective analysis Freire de Melo, Fabrício Marques, Hanna Santos Rocha Pinheiro, Samuel Luca Lemos, Fabian Fellipe Bueno Silva Luz, Marcel Nayara Teixeira, Kádima Souza, Cláudio Lima Oliveira, Márcio Vasconcelos World J Clin Oncol Review Gastric cancer is the fifth most common malignancy and third leading cancer-related cause of death worldwide. Helicobacter pylori is a Gram-negative bacterium that inhabits the gastric environment of 60.3% of the world’s population and represents the main risk factor for the onset of gastric neoplasms. CagA is the most important virulence factor in H. pylori, and is a translocated oncoprotein that induces morphofunctional modifications in gastric epithelial cells and a chronic inflammatory response that increases the risk of developing precancerous lesions. Upon translocation and tyrosine phosphorylation, CagA moves to the cell membrane and acts as a pathological scaffold protein that simultaneously interacts with multiple intracellular signaling pathways, thereby disrupting cell proliferation, differentiation and apoptosis. All these alterations in cell biology increase the risk of damaged cells acquiring pro-oncogenic genetic changes. In this sense, once gastric cancer sets in, its perpetuation is independent of the presence of the oncoprotein, characterizing a “hit-and-run” carcinogenic mechanism. Therefore, this review aims to describe H. pylori- and CagA-related oncogenic mechanisms, to update readers and discuss the novelties and perspectives in this field. Baishideng Publishing Group Inc 2022-11-24 2022-11-24 /pmc/articles/PMC9724182/ /pubmed/36483973 http://dx.doi.org/10.5306/wjco.v13.i11.866 Text en ©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved. https://creativecommons.org/licenses/by-nc/4.0/This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (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.
spellingShingle Review
Freire de Melo, Fabrício
Marques, Hanna Santos
Rocha Pinheiro, Samuel Luca
Lemos, Fabian Fellipe Bueno
Silva Luz, Marcel
Nayara Teixeira, Kádima
Souza, Cláudio Lima
Oliveira, Márcio Vasconcelos
Influence of Helicobacter pylori oncoprotein CagA in gastric cancer: A critical-reflective analysis
title Influence of Helicobacter pylori oncoprotein CagA in gastric cancer: A critical-reflective analysis
title_full Influence of Helicobacter pylori oncoprotein CagA in gastric cancer: A critical-reflective analysis
title_fullStr Influence of Helicobacter pylori oncoprotein CagA in gastric cancer: A critical-reflective analysis
title_full_unstemmed Influence of Helicobacter pylori oncoprotein CagA in gastric cancer: A critical-reflective analysis
title_short Influence of Helicobacter pylori oncoprotein CagA in gastric cancer: A critical-reflective analysis
title_sort influence of helicobacter pylori oncoprotein caga in gastric cancer: a critical-reflective analysis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9724182/
https://www.ncbi.nlm.nih.gov/pubmed/36483973
http://dx.doi.org/10.5306/wjco.v13.i11.866
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