ArticleOncogene2005
Transformed immortalized gastric epithelial cells by virulence factor CagA of Helicobacter pylori through Erk mitogen-activated protein kinase pathway.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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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.
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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
30 citing papers in PubMed, 60 citations in OpenAlex.
- Prevalence and correlation with clinical diseases of Helicobacter pylori cagA and vacA genotype among gastric patients from Northeast China.BioMed research international · 2014Trial
- The Antithetic Roles of IQGAP2 and IQGAP3 in Cancers.Cancers · 2023Review
- Review
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- MicroRNA Modulation of Host Immune Response and Inflammation Triggered byInternational journal of molecular sciences · 2021Review
- Helicobacter pylori pathogen regulates p14ARF tumor suppressor and autophagy in gastric epithelial cells.Oncogene · 2018Article
- A SystematicCurrent genomics · 2017Article
- Article
- Fucosyltransferase-4 and Oligosaccharide Lewis Y Antigen as potentially Correlative Biomarkers of Helicobacter pylori CagA Associated Gastric Cancer.Pathology oncology research : POR · 2017Article
- Differences in TGF-β1 signaling and clinicopathologic characteristics of histologic subtypes of gastric cancer.BMC cancer · 2016Article
- Helicobacter pylori-induced inflammation and epigenetic changes during gastric carcinogenesis.World journal of gastroenterology · 2015Review
- Helicobacter pylori and microRNAs: Relation with innate immunity and progression of preneoplastic conditions.World journal of clinical oncology · 2015Review
- Microbial Regulation of p53 Tumor Suppressor.PLoS pathogens · 2015Review
- Article
- A specific A/T polymorphism in Western tyrosine phosphorylation B-motifs regulates Helicobacter pylori CagA epithelial cell interactions.PLoS pathogens · 2015Article
- Helicobacter pylori and interleukin-8 in gastric cancer.World journal of gastroenterology · 2013Review
- Helicobacter pylori-induced alteration of epithelial cell signaling and polarity: a possible mechanism of gastric carcinoma etiology and disparity.Cytoskeleton (Hoboken, N.J.) · 2013Review
- Helicobacter pylori CagA: a critical destroyer of the gastric epithelial barrier.Digestive diseases and sciences · 2013Review
- MicroRNAs up-regulated by CagA of Helicobacter pylori induce intestinal metaplasia of gastric epithelial cells.PloS one · 2012Article
- Helicobacter pylori CagA triggers expression of the bactericidal lectin REG3γ via gastric STAT3 activation.PloS one · 2012Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CagA of Helicobacter pylori is a protein that has been closely associated with gastric cancer and that can intervene with signal pathways in cells. Its precise relationship with the occurrence of gastric cancer, however, remains unclear. The purpose of this study is to investigate whether CagA can promote transformation of normal gastric epithelial cells and to consider via what mechanisms CagA may exert its effects. Transformed colonies were merged in soft-agarose medium after immortalized gastric epithelial cells were transfected with recombinant pLHCX retrovirus with cagA and/or dimethylhydrazine. The number of transformed colonies in the group containing cagA/pLHCX retrovirus, combined with a subthreshold dose of dimethylhydrazine, was more than that for cagA/pLHCX retrovirus or dimethylhydrazine at a subthreshold dose alone. For cagA-transfected cells, only IQGAP-2, R-Ras and B-Raf of the Ras/mitogen-activated protein kinase signal pathway were markedly increased, and the activity of extracellular signal-regulated kinase 1/2 (Erk1/2) kinase was significantly higher than that in dimethylhydrazine-transformed cells or control cells. However, no evidence of alteration of any other molecules of the Ras superfamily was observed in cagA-transfected cells. These findings suggest that CagA can transform gastric epithelial cells through activation of the Erk1/2 pathway; this mechanism may, however, be independent of Ras activation.
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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.