Helicobacter pylori regulates stomach diseases by activating cell pathways and DNA methylation of host cells
One of the most prevalent malignant tumors of the digestive tract is gastric cancer (GC). Age, high salt intake, Helicobacter pylori (H. pylori) infection, and a diet deficient in fruits and vegetables are risk factors for the illness. A significant risk factor for gastric cancer is infection with H...
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Frontiers Media S.A.
2023-05-01
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Series: | Frontiers in Cell and Developmental Biology |
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Online Access: | https://www.frontiersin.org/articles/10.3389/fcell.2023.1187638/full |
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author | Yue Xi Xiao-Li Zhang Qing-Xin Luo Hai-Ning Gan Yu-Shi Liu Shi-He Shao Xu-Hua Mao |
author_facet | Yue Xi Xiao-Li Zhang Qing-Xin Luo Hai-Ning Gan Yu-Shi Liu Shi-He Shao Xu-Hua Mao |
author_sort | Yue Xi |
collection | DOAJ |
description | One of the most prevalent malignant tumors of the digestive tract is gastric cancer (GC). Age, high salt intake, Helicobacter pylori (H. pylori) infection, and a diet deficient in fruits and vegetables are risk factors for the illness. A significant risk factor for gastric cancer is infection with H. pylori. Infecting gastric epithelial cells with virulence agents secreted by H. pylori can cause methylation of tumor genes or carcinogenic signaling pathways to be activated. Regulate downstream genes’ aberrant expression, albeit the precise mechanism by which this happens is unclear. Oncogene, oncosuppressor, and other gene modifications, as well as a number of different gene change types, are all directly associated to the carcinogenesis of gastric cancer. In this review, we describe comprehensive H. pylori and its virulence factors, as well as the activation of the NF-κB, MAPK, JAK/STAT signaling pathways, and DNA methylation following infection with host cells via virulence factors, resulting in abnormal gene expression. As a result, host-related proteins are regulated, and gastric cancer progression is influenced. This review provides insight into the H. pylori infection, summarizes a series of relevant papers, discusses the complex signaling pathways underlying molecular mechanisms, and proposes new approach to immunotherapy of this important disease. |
first_indexed | 2024-04-09T14:26:14Z |
format | Article |
id | doaj.art-9480bf5cd0c04fe98562d777f344e302 |
institution | Directory Open Access Journal |
issn | 2296-634X |
language | English |
last_indexed | 2024-04-09T14:26:14Z |
publishDate | 2023-05-01 |
publisher | Frontiers Media S.A. |
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series | Frontiers in Cell and Developmental Biology |
spelling | doaj.art-9480bf5cd0c04fe98562d777f344e3022023-05-04T04:32:35ZengFrontiers Media S.A.Frontiers in Cell and Developmental Biology2296-634X2023-05-011110.3389/fcell.2023.11876381187638Helicobacter pylori regulates stomach diseases by activating cell pathways and DNA methylation of host cellsYue Xi0Xiao-Li Zhang1Qing-Xin Luo2Hai-Ning Gan3Yu-Shi Liu4Shi-He Shao5Xu-Hua Mao6School of Medicine, Jiangsu University, Zhenjiang, ChinaDepartment of Clinical Laboratory, The Affiliated Yixing Hospital of Jiangsu University, Wuxi, ChinaSchool of Medicine, Jiangsu University, Zhenjiang, ChinaSchool of Medicine, Jiangsu University, Zhenjiang, ChinaSchool of Medicine, Jiangsu University, Zhenjiang, ChinaSchool of Medicine, Jiangsu University, Zhenjiang, ChinaDepartment of Clinical Laboratory, The Affiliated Yixing Hospital of Jiangsu University, Wuxi, ChinaOne of the most prevalent malignant tumors of the digestive tract is gastric cancer (GC). Age, high salt intake, Helicobacter pylori (H. pylori) infection, and a diet deficient in fruits and vegetables are risk factors for the illness. A significant risk factor for gastric cancer is infection with H. pylori. Infecting gastric epithelial cells with virulence agents secreted by H. pylori can cause methylation of tumor genes or carcinogenic signaling pathways to be activated. Regulate downstream genes’ aberrant expression, albeit the precise mechanism by which this happens is unclear. Oncogene, oncosuppressor, and other gene modifications, as well as a number of different gene change types, are all directly associated to the carcinogenesis of gastric cancer. In this review, we describe comprehensive H. pylori and its virulence factors, as well as the activation of the NF-κB, MAPK, JAK/STAT signaling pathways, and DNA methylation following infection with host cells via virulence factors, resulting in abnormal gene expression. As a result, host-related proteins are regulated, and gastric cancer progression is influenced. This review provides insight into the H. pylori infection, summarizes a series of relevant papers, discusses the complex signaling pathways underlying molecular mechanisms, and proposes new approach to immunotherapy of this important disease.https://www.frontiersin.org/articles/10.3389/fcell.2023.1187638/fullHelicobacter pylorisignaling pathwayapoptosisDNA methylationgastric cancer |
spellingShingle | Yue Xi Xiao-Li Zhang Qing-Xin Luo Hai-Ning Gan Yu-Shi Liu Shi-He Shao Xu-Hua Mao Helicobacter pylori regulates stomach diseases by activating cell pathways and DNA methylation of host cells Frontiers in Cell and Developmental Biology Helicobacter pylori signaling pathway apoptosis DNA methylation gastric cancer |
title | Helicobacter pylori regulates stomach diseases by activating cell pathways and DNA methylation of host cells |
title_full | Helicobacter pylori regulates stomach diseases by activating cell pathways and DNA methylation of host cells |
title_fullStr | Helicobacter pylori regulates stomach diseases by activating cell pathways and DNA methylation of host cells |
title_full_unstemmed | Helicobacter pylori regulates stomach diseases by activating cell pathways and DNA methylation of host cells |
title_short | Helicobacter pylori regulates stomach diseases by activating cell pathways and DNA methylation of host cells |
title_sort | helicobacter pylori regulates stomach diseases by activating cell pathways and dna methylation of host cells |
topic | Helicobacter pylori signaling pathway apoptosis DNA methylation gastric cancer |
url | https://www.frontiersin.org/articles/10.3389/fcell.2023.1187638/full |
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