NF-kB-dependent activation of STAT3 by H. pylori is suppressed by TFF1

Soutto, Mohammed; Bhat, Nadeem S.; Khalafi, Shayan; Zhu, Shoumin; Poveda, Julio; García-Buitrago, Mónica; Zaika, Alexander; El–Rifai, Wael

doi:10.1186/s12935-021-02140-2

Cited by 17 publications

(4 citation statements)

References 51 publications

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“…However, this pathway is hijacked by neoplastic cells during carcinogenesis, thus promoting growth, survival, angiogenesis, and metastasis [ 112 ]. Furthermore, there is constitutive activation of STAT3 signaling in cancer that inhibits both apoptosis and antitumor immunity [ 113 , 114 ] (Fig. 2 A).…”

Section: Role Of Chronic Inflammation In the Development Of Ecmentioning

confidence: 99%

Cross-talk between the microbiome and chronic inflammation in esophageal cancer: potential driver of oncogenesis

Sharma

Gupta

Chauhan

et al. 2022

Cancer Metastasis Rev

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Esophageal cancer (EC) is frequently considered a lethal malignancy and is often identified at a later stage. It is one of the major causes of cancer-related deaths globally. The conventional treatment methods like chemotherapy, radiotherapy, and surgery offer limited efficacy and poor clinical outcome with a less than 25% 5-year survival rate. The poor prognosis of EC persists despite the growth in the development of diagnostic and therapeutic modalities to treat EC. This underlines the need to elucidate the complex molecular mechanisms that drive esophageal oncogenesis. Apart from the role of the tumor microenvironment and its structural and cellular components in tumorigenesis, mounting evidence points towards the involvement of the esophageal microbiome, inflammation, and their cross-talk in promoting esophageal cancer. The current review summarizes recent research that delineates the underlying molecular mechanisms by which the microbiota and inflammation promote the pathophysiology of esophageal cancer, thus unraveling targets for potential therapeutic intervention.

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Section: Role Of Chronic Inflammation In the Development Of Ecmentioning

confidence: 99%

Cross-talk between the microbiome and chronic inflammation in esophageal cancer: potential driver of oncogenesis

Sharma

Gupta

Chauhan

et al. 2022

Cancer Metastasis Rev

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“…Such capability provides both the avenue and the mechanism for H. pylori, a recognized group 1 carcinogen, to induce chronic inflammation and malignancy in the hepatobiliary system [10]. Mechanistically, H. pylori triggers multiple oncogenic, intracellular pathways within epithelial cells, including phosphoinositide-3-kinase (PI3K), nuclear factor kappa B (NF-κB), and Wnt/β-catenin [25][26][27]. These pathways influence various cellular functions, leading to the heightened production of inflammatory cytokines, altered apoptosis rates, and enhanced epithelial cell proliferation and differentiation, ultimately culminating in the oncogenic transformation of biliary epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

Exploring the Relationship Between Helicobacter pylori Infection and Biliary Diseases: A Comprehensive Analysis Using the United States National Inpatient Sample (2016-2020)

Ahmad,

AlAmr,

Taftafa

et al. 2024

Cureus

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Background: Helicobacter pylori (H. pylori) infection is widely recognized for its association with gastric diseases. Prior studies on the relationship between H. pylori infection and biliary diseases have faced constraints, including inadequate control of confounding factors and small sample sizes. This study aims to explore the association between H. pylori infection and biliary diseases using a large, population-based sample with adequate control for various covariates.Methods: The National Inpatient Sample (NIS) from 2016 to 2020 was used to investigate the association between H. pylori infection and biliary diseases. We identified patients with H. pylori infection using the International Classification of Diseases, Tenth Revision (ICD-10) code (B96.81). Descriptive analysis and inferential statistics, including univariate and multivariate regression, were performed to explore the relationship between H. pylori and selected biliary diseases.Results: Overall, 32,966,720 patients were analyzed. Among them, 736,585 patients had biliary diseases (n=1,637 with H. pylori and n=734,948 without H. pylori). The baseline characteristics revealed notable differences in demographics and healthcare variables between both groups. Univariate regression analysis demonstrated significant associations between H. pylori infection and various biliary diseases such as gallbladder stones, gallbladder cancer, cholangitis, acute cholecystitis, and biliary pancreatitis, with the highest risk for chronic cholecystitis (odds ratio: 5.21; 95% confidence interval: 4.1-6.62; p<0.0001). Multivariate regression analysis, after adjusting for various covariates, confirmed these associations, providing insights into the potential causal relationship between H. pylori and biliary diseases.Conclusion: This study strengthens the evidence suggesting a potential association between H. pylori infection and biliary diseases. The findings need to be validated in prospective clinical studies.

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“…One of the molecular mechanisms revealing the anti-inflammatory activity of TFF1 during H. pylori infection has been recently reported by Soutto et al ., who showed a reduced NFkB-dependent STAT3 activation promoted by TFF1 [32].…”

Section: Discussionmentioning

confidence: 99%

IFNγ-dependent silencing of TFF1 during Helicobacter pylori infection

et al. 2022

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Chronic Helicobacter pylori infection is the leading cause of intestinal-type adenocarcinoma, as prolonged Helicobacter colonization triggers chronic active gastritis, which may evolve into adenocarcinoma of the intestinal type. In this environment, cytokines play a significant role in determining the evolution of the infection. In combination with other factors (genetic, environmental and nutritional), the pro-inflammatory response may trigger pro-oncogenic mechanisms that lead to the silencing of tumour-suppressor genes, such as trefoil factor 1 (TFF1). The latter is known to play a protective role by maintaining the gastric mucosa integrity and retaining H. pylori in the mucus layer, preventing the progression of infection and, consequently, the development of gastric cancer (GC). Since TFF1 expression is reduced during chronic Helicobacter infection with a loss of gastric mucosa protection, we investigated the molecular pathways involved in this reduction. Specifically, we evaluated the effect of some pro-inflammatory cytokines on TFF1 regulation in GC and primary gastric cells by RT-qPCR and luciferase reporter assay analyses and the repressor role of the transcription factor C/EBPβ, overexpressed in gastric-intestinal cancer. Our results show that, among several cytokines, IFNγ stimulates C/EBPβ expression, which acts as a negative regulator of TFF1 by binding its promoter at three different sites.

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NF-kB-dependent activation of STAT3 by H. pylori is suppressed by TFF1

Cited by 17 publications

References 51 publications

Cross-talk between the microbiome and chronic inflammation in esophageal cancer: potential driver of oncogenesis

Cross-talk between the microbiome and chronic inflammation in esophageal cancer: potential driver of oncogenesis

Exploring the Relationship Between Helicobacter pylori Infection and Biliary Diseases: A Comprehensive Analysis Using the United States National Inpatient Sample (2016-2020)

IFNγ-dependent silencing of TFF1 during Helicobacter pylori infection

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