Micro<scp>RNA</scp>‐3178 ameliorates inflammation and gastric carcinogenesis promoted by <i><scp>H</scp>elicobacter pylori</i> new toxin, Tip‐α, by targeting <scp>TRAF</scp>3

Zou, Meijuan; Wang, Fang; Jiang, Aiqin; Xia, Anliang; Kong, Siya; Gong, Chun; Zhu, Mingxia; Zhou, Xin; Zhu, Jun; Zhu, Wei; Cheng, Wenfang

doi:10.1111/hel.12348

Cited by 28 publications

(24 citation statements)

References 46 publications

(90 reference statements)

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“…It makes up one of the potential markers of H. pylori virulence [164,165]. By combining with the nucleolin receptor, Tipα induces mesenchymal changes of cells via EMT progression [166][167][168]. Tipα, as a carcinogenic factor, activates NF-κB, promoting gastric carcinogenesis by inhibiting miR-3178 expression [169,170].…”

Section: Tumor Necrosis Factor α-Inducing Protein Of H Pylori In Emtmentioning

confidence: 99%

Mechanisms of the Epithelial–Mesenchymal Transition and Tumor Microenvironment in Helicobacter pylori-Induced Gastric Cancer

Baj

Korona-Głowniak

Forma

et al. 2020

Cells

124

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Helicobacter pylori (H. pylori) is one of the most common human pathogens, affecting half of the world's population. Approximately 20% of the infected patients develop gastric ulcers or neoplastic changes in the gastric stroma. An infection also leads to the progression of epithelial-mesenchymal transition within gastric tissue, increasing the probability of gastric cancer development. This paper aims to review the role of H. pylori and its virulence factors in epithelial-mesenchymal transition associated with malignant transformation within the gastric stroma. The reviewed factors included: CagA (cytotoxin-associated gene A) along with induction of cancer stem-cell properties and interaction with YAP (Yes-associated protein pathway), tumor necrosis factor α-inducing protein, Lpp20 lipoprotein, Afadin protein, penicillin-binding protein 1A, microRNA-29a-3p, programmed cell death protein 4, lysosomal-associated protein transmembrane 4β, cancer-associated fibroblasts, heparin-binding epidermal growth factor (HB-EGF), matrix metalloproteinase-7 (MMP-7), and cancer stem cells (CSCs). The review summarizes the most recent findings, providing insight into potential molecular targets and new treatment strategies for gastric cancer.

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Section: Tumor Necrosis Factor α-Inducing Protein Of H Pylori In Emtmentioning

confidence: 99%

Mechanisms of the Epithelial–Mesenchymal Transition and Tumor Microenvironment in Helicobacter pylori-Induced Gastric Cancer

Baj

Korona-Głowniak

Forma

et al. 2020

Cells

124

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“…Regarding H. pylori ‐related virulence factors, Zou et al. demonstrated that Tip‐α, a carcinogenic factor of H. pylori , activated NF‐κB by inhibiting the miR‐3178‐mediated targeting of TRAF3 . MiR‐124 has tumor suppressive functions and is regulated by CpG methylation silencing .…”

Section: Deregulation Of Host Functionsmentioning

confidence: 99%

“…46 Regarding H. pylori-related virulence factors, Zou et al demonstrated that Tipα, a carcinogenic factor of H. pylori, activated NF-κB by inhibiting the miR-3178-mediated targeting of TRAF3. 47 MiR-124 has tumor suppressive functions and is regulated by CpG methylation silencing. 48 Murray-Stewart et al reported that miR-124 is a negative regulator of polyamine catabolic enzyme spermine oxidase (SMOX), which is induced in H. pylori gastritis.…”

Section: H Pylori Infection and Autophagymentioning

confidence: 99%

Pathogenesis of Helicobacter pylori infection

2017

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Helicobacter pylori is responsible for the most commonly found infection in the world's population. It is the major risk factor for gastric cancer development. Numerous studies published over the last year provide new insights into the strategies employed by H. pylori to adapt to the extreme acidic conditions of the gastric environment, to establish persistent infection and to deregulate host functions, leading to gastric pathogenesis and cancer. In this review, we report recent data on the mechanisms involved in chemotaxis, on the essential role of nickel in acid resistance and gastric colonization, on the importance of adhesins and Hop proteins and on the role of CagPAI-components and CagA. Among the host functions, a special focus has been made on the escape from immune response, the ability of bacteria to induce genetic instability and modulate telomeres, the mechanism of autophagy and the deregulation of micro RNAs.

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“…They concluded that miRNAs modulate mucosal cytokine expression and are involved in regulating gastric pathology. Zou et al . found that miR‐3178 was decreased in H. pylori‐ infected human gastric tissue, and investigated its role in regulating the inflammatory response to tumor necrosis factor‐α‐inducing protein (Tip‐α), a recently identified H. pylori toxin.…”

Section: Inflammationmentioning

confidence: 99%

“…Zou et al 15 found that miR-3178 was decreased in H. pylori-infected human gastric tissue, and investigated its role in regulating the inflammatory response to tumor necrosis factorα-inducing protein (Tipα), a recently identified H. pylori toxin. Addition of rTipα to GECs, resulted in increased TNFα and IL-6 expressions.…”

Section: Epithelial Cell -Helicobacter Pylori Interactionsmentioning

confidence: 99%

Helicobacter: Inflammation, immunology and vaccines

2017

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Helicobacter pylori is usually acquired in early childhood and the infection persists lifelong without causing symptoms. In a small of cases, the infection leads to gastric or duodenal ulcer disease, or gastric cancer. Why disease occurs in these individuals remains unclear, however the host response is known to play a very important part. Understanding the mechanisms involved in maintaining control over the immune and inflammatory response is therefore extremely important. Vaccines against H. pylori have remained elusive but are desperately needed for the prevention of gastric carcinogenesis. This review focuses on research findings which may prove useful in the development of prognostic tests for gastric cancer development, therapeutic agents to control immunopathology, and effective vaccines.

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MicroRNA‐3178 ameliorates inflammation and gastric carcinogenesis promoted by Helicobacter pylori new toxin, Tip‐α, by targeting TRAF3

Abstract: Taken all together, Tip-α might activate NF-κB to promote inflammation and carcinogenesis by inhibiting miR-3178 expression, which directly targeting TRAF3, during H. pylori infection in gastric mucosal epithelial cells.

Cited by 28 publications

References 46 publications

Mechanisms of the Epithelial–Mesenchymal Transition and Tumor Microenvironment in Helicobacter pylori-Induced Gastric Cancer

Mechanisms of the Epithelial–Mesenchymal Transition and Tumor Microenvironment in Helicobacter pylori-Induced Gastric Cancer

Pathogenesis of Helicobacter pylori infection

Helicobacter: Inflammation, immunology and vaccines

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