ArticleJournal of experimental & clinical cancer research : CR2018
Helicobacter pylori CagA promotes epithelial mesenchymal transition in gastric carcinogenesis via triggering oncogenic YAP pathway.
Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 82 papers, 1 of them a synthesis that pooled it.
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Who cites it
82 citing papers in PubMed, 1 synthesis or guideline pooled it, 142 citations in OpenAlex.
- Conservation of Epithelial-to-Mesenchymal Transition Process in Neural Crest Cells and Metastatic Cancer.Cells, tissues, organs · 2021Pooled it
- CagA promotes gastric cancer stemness and metastasis via DNMT1-mediated epigenetic silencing of BEX1.Cancer gene therapy · 2026Article
- The "Hit-and-Run" legacy: epigenetic locking and the survival switch in H. pylori-associated gastric cancer.Cell death discovery · 2026Review
- The microbiome-EBV axis in carcinogenesis bridges commensal influence and viral oncogenesis.Frontiers in immunology · 2026Review
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- Gut microbiome and nutritional strategies in gastrointestinal cancers: Clinical implications and therapeutic perspectives.World journal of clinical oncology · 2025Review
- Update on molecular pathogenesis ofWorld journal of gastrointestinal pathophysiology · 2025Review
- Helicobacter pylori activates DOPEY1 to promote p53 degradation through the USP7/TRIP12 axis in gastric tumorigenesis.Oncogene · 2025Article
- The N-terminus of theMicrobiology spectrum · 2025Article
- 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
- Digestive cancers: mechanisms, therapeutics and management.Signal transduction and targeted therapy · 2025Review
- Helicobacter pylori CagA promotes gastric cancer immune escape by upregulating SQLE.Cell death & disease · 2025Article
- Helicobacter pylori infection promotes M1 macrophage polarization and gastric inflammation by activation of NLRP3 inflammasome via TNF/TNFR1 axis.Cell communication and signaling : CCS · 2025Article
- The intersection ofFrontiers in cellular and infection microbiology · 2025Review
- The role of oral microbiota in digestive system diseases: current advances and perspectives.Journal of oral microbiology · 2025Review
- The N-terminus of thebioRxiv : the preprint server for biology · 2024Article
- Prevention of Gastric Cancer:The Korean journal of helicobacter and upper gastrointestinal research · 2024Review
- Disabled-2, a versatile tissue matrix multifunctional scaffold protein with multifaceted signaling: Unveiling its potential in the cancer battle.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Role of Helicobacter pylori virulence factors and alteration of the Tumor Immune Microenvironment: challenges and opportunities for Cancer Immunotherapy.Archives of microbiology · 2024Review
22 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundHelicobacter pylori (H. pylori) delivers oncoprotein CagA into gastric epithelial cells via the T4SS and drives activation of multiple oncogenic signalling pathways. YAP, a core effector of the Hippo tumour suppressor pathway, is frequently overexpressed in human cancers, suggesting its potential tumor-promoting role. Although CagA is a casual factor in H. pylori induced gastric carcinogenesis, the link between CagA and YAP pathway has not been identified. In this work, we investigated the regulation of oncogenic YAP pathway by H. pylori CagA.
methodsExpression of YAP and E-cadherin protein in human gastric biopsies were assessed by immunohistochemistry. H. pylori PMSS1 cagA
resultsYAP is significantly upregulated in human gastric carcinogenesis. We generated PMSS1 CagA isogenic mutant strains with chloramphenicol resistance successfully. Our analysis indicated that H. pylori infection induced YAP and downstream effectors in gastric epithelial cells. Importantly, knockout of CagA in 7.13 and PMSS1 strains reduced the expression of YAP by H. pylori infection. Moreover, Inhibition of YAP suppressed H. pylori infection-induced Epithelial-mesenchymal transition (EMT).
conclusionOur results indicated that H. pylori CagA as a pathogenic protein promotes oncogenic YAP pathway, which contributes to EMT and gastric tumorigenesis. This study provided a novel mechanistic insight into why cagA
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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.