ArticleGut2005
Transactivation of the epidermal growth factor receptor by cag+ Helicobacter pylori induces upregulation of the early growth response gene Egr-1 in gastric epithelial cells.
Article in Gut, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 48 citations in OpenAlex.
- The Salmonella pathogenicity island 1 injectisome reprograms host cell translation to evade the inflammatory response.Nature communications · 2025Article
- The composition and roles of gastric stem cells in epithelial homeostasis, regeneration, and tumorigenesis.Cellular oncology (Dordrecht, Netherlands) · 2023Review
- Acyl Homoserine Lactone Sensitised Streptococcus Pyogenes Differentially Regulates the Transcriptional Expression of Early Growth Response 1 (EGR1) in Epithelial and Macrophage Cells.Current microbiology · 2023Article
- Single-cell RNA sequencing reveals cellular and molecular reprograming landscape of gliomas and lung cancer brain metastases.Clinical and translational medicine · 2022Article
- Rapid pathogen-specific recruitment of immune effector cells in the skin by secreted toxins.Nature microbiology · 2022Article
- Early growth response 1 (EGR1) activation in initial stages of host-pathogen interactions.Molecular biology reports · 2021Review
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- The Host Cell Transcription Factor EGR1 Is Induced by Bacteria through the EGFR-ERK1/2 Pathway.Frontiers in cellular and infection microbiology · 2017Article
- Expression of early growth response gene-1 in precancerous lesions of gastric cancer.Oncology letters · 2016Article
- Wnt/β-catenin, an oncogenic pathway targeted by H. pylori in gastric carcinogenesis.Oncotarget · 2015Review
- Effect of Helicobacter pylori Infection on the Composition of Gastric Microbiota in the Development of Gastric Cancer.Gastrointestinal tumors · 2015Review
- Role of vacuolating cytotoxin VacA and cytotoxin-associated antigen CagA of Helicobacter pylori in the progression of gastric cancer.Molecular and cellular biochemistry · 2014Article
- Cyanidin 3-O-glucoside reduces Helicobacter pylori VacA-induced cell death of gastric KATO III cells through inhibition of the SecA pathway.International journal of medical sciences · 2014Article
- The Effect of Helicobacter pylori on Epidermal Growth Factor Receptor-Induced Signal Transduction and the Preventive Effect of Celecoxib in Gastric Cancer Cells.Gut and liver · 2013Article
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- Molecular Interactions between MUC1 Epithelial Mucin, β-Catenin, and CagA Proteins.Frontiers in immunology · 2012Article
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- A small fibronectin-mimicking protein from bacteria induces cell spreading and focal adhesion formation.The Journal of biological chemistry · 2010Article
- Helicobacter pylori: gastric cancer and beyond.Nature reviews. Cancer · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
BACKGROUND AND
aimsHelicobacter pylori, in particular cytotoxin associated gene (cag)+ strains, have been shown to enhance gastric epithelial cell proliferation in vivo, an effect that likely contributes to gastric carcinogenesis. Early growth response gene 1 (Egr-1) is a crucial regulator of cell growth, differentiation, and survival, which is known to play a role in carcinogenesis and cancer progression. The aims of this study were to: (1) examine whether H pylori could upregulate Egr-1 in gastric epithelial cell lines; (2) determine whether there was a differential response to infection with different strains; (3) examine the role of the cag pathogenicity island in this process; and (4) elucidate the molecular mechanisms leading to Egr-1 upregulation. METHODS AND
resultsWe found that infection of AGS cells with cag+H pylori resulted in a rapid (1-2 hours) but transient increase in Egr-1 mRNA and protein levels whereas coculture with cag- isolates did not elicit this response. Furthermore, two independent cagE- isogenic mutants of H pylori also demonstrated impaired ability to upregulate Egr-1. Upregulation of Egr-1 protein was inhibited by the extracellular regulated kinase (ERK)1/2 inhibitor PD98059 and overexpression of dominant negative MEK1 downregulated Egr-1 luciferase reporter gene activity. Treatment of AGS cells with the epidermal growth factor receptor (EGFR) kinase inhibitors PD153035 and AG1478 resulted in a reduction in H pylori mediated Egr-1 upregulation, demonstrating that EGFR transactivation plays a role in this early cellular process.
conclusionsOur findings show that cag+H pylori cause rapid induction of Egr-1 in gastric epithelial cells which may contribute to H pylori mediated pathogenesis.
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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.