ArticleCancer medicine2019
Helicobacter pylori-induced YAP1 nuclear translocation promotes gastric carcinogenesis by enhancing IL-1β expression.
Article in Cancer medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 63 citations in OpenAlex.
- Advances inOncology letters · 2026Review
- The ageing holobiont: crosstalk between telomere dynamics, oxidative stress and the gut microbiome.Biological reviews of the Cambridge Philosophical Society · 2026Review
- Knocking Down HN1 Blocks Helicobacter pylori-Induced Malignant Phenotypes in Gastric Mucosal Cells and Inhibits Gastric Cancer Cell Proliferation, Cytoskeleton Remodeling, and Migration.Biochemical genetics · 2025Article
- STAT3-mediated up-regulation of DAB2 via SRC-YAP1 signaling axis promotes Helicobacter pylori-driven gastric tumorigenesis.Biomarker research · 2024Article
- Current study of pathogenetic mechanisms and therapeutics of chronic atrophic gastritis: a comprehensive review.Frontiers in cell and developmental biology · 2024Review
- Review
- Cardiac fibroblasts and mechanosensation in heart development, health and disease.Nature reviews. Cardiology · 2023Review
- Helicobacter pylori-induced aberrant demethylation and expression of GNB4 promotes gastric carcinogenesis via the Hippo-YAP1 pathway.BMC medicine · 2023Article
- The Hippo signaling pathway in gastric cancer.Acta biochimica et biophysica Sinica · 2023Review
- New Insights into the Relationship between Gut Microbiota and Radiotherapy for Cancer.Nutrients · 2022Review
- YAP promotes cell-autonomous immune responses to tackle intracellular Staphylococcus aureus in vitro.Nature communications · 2022Article
- Targeting the Hippo Pathway in Gastric Cancer and Other Malignancies in the Digestive System: From Bench to Bedside.Biomedicines · 2022Review
- In Peripheral Blood Mononuclear CellsInternational journal of molecular sciences · 2022Article
- HIPPO signaling-related signature for predicting prognosis and therapeutic response in gastric cancer.Frontiers in pharmacology · 2022Article
- YAP1 promotes high glucose-induced inflammation and extracellular matrix deposition in glomerular mesangial cells by modulating NF-κB/JMJD3 pathway.Experimental and therapeutic medicine · 2021Article
- FRA-1 suppresses apoptosis of Helicobacter pylori infected MGC-803 cells.Molecular biology reports · 2021Article
- Association ofCanadian journal of gastroenterology & hepatology · 2021Review
- Cisplatin promotes the expression level of PD-L1 in the microenvironment of hepatocellular carcinoma through YAP1.Molecular and cellular biochemistry · 2020Article
- Interleukin-1β and Cancer.Cancers · 2020Review
- TAZ ControlsCells · 2020Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastric cancer (GC) is one of the most common and malignant pathologies, and a significant portion of GC incidences develops from Helicobacter pylori (Hp)-induced chronic gastritis. Although the exact mechanisms of GC are complex and poorly understood, gastric carcinogenesis is a good model to investigate how inflammation and infection collaboratively promote tumorigenesis. Yes-associated protein 1 (YAP1) is the key effector of the Hippo pathway, which is silenced in most human cancers. Herein, we verified the tumor-promoting effect of YAP1 in vitro, in vivo, and in human specimens. We revealed that YAP1 displays nuclear translocation and works with TEAD to activate transcription of the crucial inflammatory cytokine IL-1β in gastric cells infected with Hp. As IL-1ß accounts for inflammation-associated tumorigenesis, this process can lead to gastric carcinogenesis. Thus, in addition to activating proliferation genes, YAP1 also plays a major role in inflammation amplification by activating inflammatory cytokine genes. Excitingly, our research demonstrates that transfection of mutant plasmid YAP-5SA/S94A or addition of the drug verteporfin, both of which are thought to disrupt the YAP1-TEAD interaction, can arrest the carcinogenesis process. These findings can provide new approaches to GC treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.