Infection of Helicobacter pylori contributes to the progression of gastric cancer through ferroptosis

Abstract Helicobacter pylori (H. pylori) is a gram-negative pathogen that colonizes gastric epithelial cells, and its chronic infection is the primary risk factor for the development of gastric cancer (GC). Ferroptosis is an iron-dependent form of cell death characterized by intracellular lipid pero...

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Main Authors: Yun Liu, Renjie Miao, Jinxuan Xia, Yong Zhou, Jun Yao, Shihe Shao
Format: Article
Language:English
Published: Nature Publishing Group 2024-12-01
Series:Cell Death Discovery
Online Access:https://doi.org/10.1038/s41420-024-02253-3
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author Yun Liu
Renjie Miao
Jinxuan Xia
Yong Zhou
Jun Yao
Shihe Shao
author_facet Yun Liu
Renjie Miao
Jinxuan Xia
Yong Zhou
Jun Yao
Shihe Shao
author_sort Yun Liu
collection DOAJ
description Abstract Helicobacter pylori (H. pylori) is a gram-negative pathogen that colonizes gastric epithelial cells, and its chronic infection is the primary risk factor for the development of gastric cancer (GC). Ferroptosis is an iron-dependent form of cell death characterized by intracellular lipid peroxide accumulation and reactive oxygen species (ROS) imbalance. There is evidence suggesting that pathogens can manipulate ferroptosis to facilitate their replication, transmission, and pathogenesis. However, the interaction between ferroptosis and H. pylori infection requires further elucidation. We reviewed the mechanism of ferroptosis and found that H. pylori virulence factors such as cytotoxin-associated gene A (CagA), vacuolating cytotoxin A (VacA), neutrophil-activating protein A (NapA), superoxide dismutase B (SodB), γ-glutamyl transpeptidase (gGT), lipopolysaccharide (LPS), and outer inflammatory protein A (OipA) affected glutathione (GSH), ROS, and lipid oxidation to regulate ferroptosis. It also affected the progression of GC by regulating ferroptosis-related indicators through abnormal gene expression after H. pylori infected gastric mucosa cells. Finally, we discuss the potential application value of ferroptosis inducers, inhibitors and other drugs in treating H. pylori-infected GC patients while acknowledging that their interactions are still not fully understood.
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spelling doaj-art-eddc6f079db14aac931d6f5835bed19a2024-12-08T12:18:40ZengNature Publishing GroupCell Death Discovery2058-77162024-12-0110111010.1038/s41420-024-02253-3Infection of Helicobacter pylori contributes to the progression of gastric cancer through ferroptosisYun Liu0Renjie Miao1Jinxuan Xia2Yong Zhou3Jun Yao4Shihe Shao5Department of Gastroenterology, Institute of Digestive Disease, The Affiliated People’s Hospital, Jiangsu UniversityDepartment of Clinical laboratory, Affiliated Third Hospital of Zhenjiang to Jiangsu UniversityZhenjiang Mental Health CenterDepartment of Gastroenterology, Institute of Digestive Disease, The Affiliated People’s Hospital, Jiangsu UniversityDepartment of Gastroenterology, Institute of Digestive Disease, The Affiliated People’s Hospital, Jiangsu UniversitySchool of Medicine, Jiangsu UniversityAbstract Helicobacter pylori (H. pylori) is a gram-negative pathogen that colonizes gastric epithelial cells, and its chronic infection is the primary risk factor for the development of gastric cancer (GC). Ferroptosis is an iron-dependent form of cell death characterized by intracellular lipid peroxide accumulation and reactive oxygen species (ROS) imbalance. There is evidence suggesting that pathogens can manipulate ferroptosis to facilitate their replication, transmission, and pathogenesis. However, the interaction between ferroptosis and H. pylori infection requires further elucidation. We reviewed the mechanism of ferroptosis and found that H. pylori virulence factors such as cytotoxin-associated gene A (CagA), vacuolating cytotoxin A (VacA), neutrophil-activating protein A (NapA), superoxide dismutase B (SodB), γ-glutamyl transpeptidase (gGT), lipopolysaccharide (LPS), and outer inflammatory protein A (OipA) affected glutathione (GSH), ROS, and lipid oxidation to regulate ferroptosis. It also affected the progression of GC by regulating ferroptosis-related indicators through abnormal gene expression after H. pylori infected gastric mucosa cells. Finally, we discuss the potential application value of ferroptosis inducers, inhibitors and other drugs in treating H. pylori-infected GC patients while acknowledging that their interactions are still not fully understood.https://doi.org/10.1038/s41420-024-02253-3
spellingShingle Yun Liu
Renjie Miao
Jinxuan Xia
Yong Zhou
Jun Yao
Shihe Shao
Infection of Helicobacter pylori contributes to the progression of gastric cancer through ferroptosis
Cell Death Discovery
title Infection of Helicobacter pylori contributes to the progression of gastric cancer through ferroptosis
title_full Infection of Helicobacter pylori contributes to the progression of gastric cancer through ferroptosis
title_fullStr Infection of Helicobacter pylori contributes to the progression of gastric cancer through ferroptosis
title_full_unstemmed Infection of Helicobacter pylori contributes to the progression of gastric cancer through ferroptosis
title_short Infection of Helicobacter pylori contributes to the progression of gastric cancer through ferroptosis
title_sort infection of helicobacter pylori contributes to the progression of gastric cancer through ferroptosis
url https://doi.org/10.1038/s41420-024-02253-3
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