ArticleCancer cell international2021
NF-kB-dependent activation of STAT3 by H. pylori is suppressed by TFF1.
Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Pooled it
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- Characterization of Monomeric and Dimeric Forms of the Lectin TFF1 in the Human Vagina: Possible Role for the Innate Immune Defence.International journal of molecular sciences · 2026Article
- Helicobacter pylori promotes gastric cancer progression via UPP1-mediated uridine bypass of glycolysis.Cancer cell international · 2026Article
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- Disruption of the biorhythm in gastric epithelial cell triggers inflammation in Helicobacter pylori-associated gastritis by aberrantly regulating NFIL3 via CagA activated ERK-SP1 pathway.Cell communication and signaling : CCS · 2025Article
- Bioaccessible Bread Melanoidins Modulate Oxidative Stress, Reduce Inflammation and Suppress Adhesion ofNutrients · 2025Article
- Research advances in the pathogenesis and therapeutic interventions of Helicobacter pylori and atrial fibrillation.Frontiers in cardiovascular medicine · 2025Review
- Inflammatory bowel disease, colitis, and cancer: unmasking the chronic inflammation link.International journal of colorectal disease · 2024Review
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- Gastric intestinal metaplasia: progress and remaining challenges.Journal of gastroenterology · 2024Review
- EGLN3 attenuates gastric cancer cell malignant characteristics by inhibiting JMJD8/NF-κB signalling activation independent of hydroxylase activity.British journal of cancer · 2024Article
- Impact ofFrontiers in gastroenterology (Lausanne, Switzerland) · 2024Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundH. pylori infection is the main risk factor for gastric cancer. In this study, we investigated H. pylori-mediated activation of STAT3 and NF-κB in gastric cancer, using in vitro and in vivo models.
methodsTo investigate the activation of NF-κB and STAT3 by H. pylori strains we used in vitro and in vivo mouse models, western blots, immunofluorescence, ChIP Assay, luciferase and quantitative real-time PCR assays.
resultsFollowing infection with H. pylori in vitro, we found an earlier phosphorylation of NF-kB-p65 (S536), followed by STAT3 (Y705). Immunofluorescence, using in vitro and in vivo models, demonstrated nuclear localization of NF-kB and STAT3, following H. pylori infection. NF-kB and STAT3 luciferase reporter assays confirmed earlier activation of NF-kB followed by STAT3. In vitro and in vivo models demonstrated induction of mRNA expression of IL-6 (p < 0.001), VEGF-α (p < 0.05), IL-17 (p < 0.001), and IL-23 (p < 0.001). Using ChIP, we confirmed co-binding of both NF-kB-p65 and STAT3 on the IL6 promoter. The reconstitution of Trefoil Factor 1 (TFF1) suppressed activation of NF-kB with reduction in IL6 levels and STAT3 activity, in response to H. pylori infection. Using pharmacologic (BAY11-7082) and genetic (IκB super repressor (IκBSR)) inhibitors of NF-kB-p65, we confirmed the requirement of NF-kB-p65 for activation of STAT3, as measured by phosphorylation, transcription activity, and nuclear localization of STAT3 in in vitro and in vivo models.
conclusionOur findings suggest the presence of an early autocrine NF-kB-dependent activation of STAT3 in response to H. pylori infection. TFF1 acts as an anti-inflammatory guard against H. pylori-mediated activation of pro-inflammatory networks.
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