Helicobacter pylori-induced NF-κB: trailblazer for gastric pathophysiology

Maubach, Gunter; Boccellato, Francesco; Naumann, Michael

doi:10.1016/j.molmed.2021.12.005

Cited by 29 publications

(15 citation statements)

References 93 publications

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“…By inducing the transcription of multiple key genes, the activation of the NF-κB signal can regulate important biological processes, such as proliferation, epithelial-mesenchymal transition, metastasis, and angiogenesis [ 28 , 29 , 30 ]. Maubach G. et al discovered that Helicobacter pylori induces gastric carcinogenesis by activating NF-κB [ 31 ]. The role of the RIPK4-NF-κB axis in promoting the invasiveness of urothelial bladder carcinoma, and a promising therapy of delivery of RIPK4 small interfering RNA for bladder cancer, was reported by Jian Ye Liu et al [ 11 , 32 ].…”

Section: Discussionmentioning

confidence: 99%

LncRNA LINC01537 Promotes Gastric Cancer Metastasis and Tumorigenesis by Stabilizing RIPK4 to Activate NF-κB Signaling

Zhong

Tan

Huang

et al. 2022

Cancers

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Many studies reported that long noncoding RNAs (lncRNAs) play a critical role in gastric cancer (GC) metastasis and tumorigenesis. However, the underlying mechanisms of lncRNAs in GC remain unexplored to a great extent. LINC01537 expression level was detected using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC). Its biological roles in GC were then investigated using functional experiments. In order to investigate the underlying mechanism of LINC01537 in GC, RNA pull-down, RNA immunoprecipitation, and ubiquitination assays were performed. LINC01537 was significantly overexpressed in GC tissues and associated with a poor prognosis. Functional experimental results revealed that LINC01537 promoted the proliferation, invasion, and migration of GC cells. The animal experiments revealed that LINC01537 promoted tumorigenesis and metastasis in vivo. Mechanistically, LINC01537 stabilizes RIPK4 by reducing the binding of RIPK4 to TRIM25 and reducing its ubiquitination degradation, thereby promoting the expression of the NF-κB signaling pathway. According to our findings, the LINC01537-RIPK4-NF-κB axis promoted GC metastasis and tumorigenesis.

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Section: Discussionmentioning

confidence: 99%

LncRNA LINC01537 Promotes Gastric Cancer Metastasis and Tumorigenesis by Stabilizing RIPK4 to Activate NF-κB Signaling

Zhong

Tan

Huang

et al. 2022

Cancers

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“…The variety of proteases involved and the diversity of protease substrates draws a complicated picture of interdependent disease mechanisms. The advent of organoid-based models and stomach-on-a-chip technologies might help to clarify the proteolytic contribution of the individual cells types present in the mucosal microenvironment of the stomach [ 139 ]. Nevertheless, targeting individual proteases could provide us with alternative strategies to fight H. pylori -associated disease and gastric cancer.…”

Section: Discussionmentioning

confidence: 99%

“…Putative Target Importance Neoplastic Transformation, Proliferation, and Cell Survival ADAM9 and -15 gastric cancer cell lines proliferation [117] ADAM10 Notch1 [67] stem-like phenotype in cancer stem cells and supports anchorage independent growth [67] ADAM12 decreases gastric cancer cell lines proliferation [117] ADAM17 HB-EGF [53] Notch1 [67] reduces apoptosis [135], poor prognosis in gastric cancer [133], induces pro-survival signaling via the EGFR [44,135,136], cancer stem like phenotype, anchorage-independent growth [67] MMP7 (matrilysin-1) promotes proliferation in non-transformed epithelial cells [132] MMP12 (macrophage metalloelastase) inversely correlates with disease outcome [37,134] caspase-3 executioner caspase, activation by caspase-8, -9, or -10 [139], activation induced by H. pylori LPS and induced MMP9 [140], H. pylori induction of anti-apoptotic proteins of the cIAP family to reduce caspase-3-dependent apoptosis [141,142] caspase-8 initiator caspase, limited proteolytic (including autocatalytic) activity, engaged by death receptors, including tumor necrosis factor receptor 1 (TNFR1) and Fas/CD95 [139], TieA-protein-induced apoptosis [143] HtrA HtrA L171 variant was enriched in gastric cancer patients and may increase efficiency in basolateral CagA delivery by H pylori and risk for developing gastric cancer [59] Table 2. Cont.…”

Section: Group/proteasementioning

confidence: 99%

Proteolytic Landscapes in Gastric Pathology and Cancerogenesis

Bernegger

Jarzab

Weßler

et al. 2022

IJMS

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Gastric cancer is a leading cause of cancer-related death, and a large proportion of cases are inseparably linked to infections with the bacterial pathogen and type I carcinogen Helicobacter pylori. The development of gastric cancer follows a cascade of transformative tissue events in an inflammatory environment. Proteases of host origin as well as H. pylori-derived proteases contribute to disease progression at every stage, from chronic gastritis to gastric cancer. In the present article, we discuss the importance of (metallo-)proteases in colonization, epithelial inflammation, and barrier disruption in tissue transformation, deregulation of cell proliferation and cell death, as well as tumor metastasis and neoangiogenesis. Proteases of the matrix metalloproteinase (MMP) and a disintegrin and metalloproteinase domain-containing protein (ADAM) families, caspases, calpain, and the H. pylori proteases HtrA, Hp1012, and Hp0169 cleave substrates including extracellular matrix molecules, chemokines, and cytokines, as well as their cognate receptors, and thus shape the pathogenic microenvironment. This review aims to summarize the current understanding of how proteases contribute to disease progression in the gastric compartment.

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“…Immunologically, it can evade host immune clearance and persistently colonize the niches, ultimately leading to the activation of pattern recognition receptors on antigen-presenting cells, gastric epithelial cells, and neutrophils [ 7 ]. In addition, H. pylori induces the activation of NF- κ B of gastric epithelial cells and leukocytes [ 7 ], contributing to the long-term colonization of H. pylori , chronic inflammatory microenvironment, and abnormal apoptosis, which further leads to accumulating mutations and malignant transformation of gastric epithelial cells [ 8 , 9 ]. However, senescence associated with aging and chronic inflammation may contribute to the neoplastic transformation [ 9 , 10 ].…”

Section: Introductionmentioning

confidence: 99%

Detection and Treatment of Helicobacter pylori: Problems and Advances

Yang

Guan

2022

Gastroenterology Research and Practice

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Helicobacter pylori (H. pylori) infection is chronic and etiologically linked to gastric cancer (GC) derived from gastric epithelium. The potential mechanism is complex, covering chronic inflammation, epithelial senescence, NF-κB activation, the cytotoxin-associated gene A protein translocation, and related abnormal signaling pathways. In clinical practice, the test-and-treat strategy, endoscopy-based strategy, and (family-based) screen-and-treat strategy are recommended to detect H. pylori and prevent GC. It has been demonstrated that the decreasing annual incidence of GC is largely attributable to the management of H. pylori. This study reviews the current clinical practice of H. pylori on the detection and eradication, alternative treatment strategies, and related problems and advances, and hopes to contribute to the better clinical management of H. pylori.

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Helicobacter pylori-induced NF-κB: trailblazer for gastric pathophysiology

Cited by 29 publications

References 93 publications

LncRNA LINC01537 Promotes Gastric Cancer Metastasis and Tumorigenesis by Stabilizing RIPK4 to Activate NF-κB Signaling

LncRNA LINC01537 Promotes Gastric Cancer Metastasis and Tumorigenesis by Stabilizing RIPK4 to Activate NF-κB Signaling

Proteolytic Landscapes in Gastric Pathology and Cancerogenesis

Detection and Treatment of Helicobacter pylori: Problems and Advances

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