ArticleCarcinogenesis2014
Gastrokine 1 inhibits the carcinogenic potentials of Helicobacter pylori CagA.
Article in Carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 41 citations in OpenAlex.
- Gastrokine 1 transferred by gastric cancer exosomes inhibits growth and invasion of gastric cancer cells in vitro and in vivo.Journal of cell communication and signaling · 2024Article
- Review
- Helicobacter pylori CagA promotes immune evasion of gastric cancer by upregulating PD-L1 level in exosomes.iScience · 2023Article
- Article
- Reactive Oxygen Species andAntioxidants (Basel, Switzerland) · 2023Review
- Review
- Metformin attenuates synergic effect of diabetes mellitus and Helicobacter pylori infection on gastric cancer cells proliferation by suppressing PTEN expression.Journal of cellular and molecular medicine · 2021Article
- Integrated analysis identifies oxidative stress genes associated with progression and prognosis in gastric cancer.Scientific reports · 2021Article
- Association ofCanadian journal of gastroenterology & hepatology · 2021Review
- Uptake and tumor-suppressive pathways of exosome-associated GKN1 protein in gastric epithelial cells.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2020Article
- Helicobacter pylori infection leads to KLF4 inactivation in gastric cancer through a TET1-mediated DNA methylation mechanism.Cancer medicine · 2020Article
- Epigenetic downregulation of MUC17 by H. pylori infection facilitates NF-κB-mediated expression of CEACAM1-3S in human gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2019Article
- Penicillin‑binding protein 1A mutation‑positive Helicobacter pylori promotes epithelial‑mesenchymal transition in gastric cancer via the suppression of microRNA‑134.International journal of oncology · 2019Article
- NKX6.3 protects against gastric mucosal atrophy by downregulating β-amyloid production.World journal of gastroenterology · 2019Article
- The role and diagnostic potential of gastrokine 1 in gastric cancer.Cancer management and research · 2019Review
- Reactive Oxygen Species Are Involved in the Development of Gastric Cancer and Gastric Cancer-Related Depression through ABL1-Mediated Inflammation Signaling Pathway.Oxidative medicine and cellular longevity · 2019Article
- Multiple genetic mutations caused by NKX6.3 depletion contribute to gastric tumorigenesis.Scientific reports · 2018Article
- Evaluation of GKN1 and GKN2 gene expression as a biomarker of gastric cancer.Gastroenterology and hepatology from bed to bench · 2018Article
- Article
- CagA promotes proliferation and inhibits apoptosis of GES-1 cells by upregulating TRAF1/4-1BB.Molecular medicine reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Helicobacter pylori CagA directly injected by the bacterium into epithelial cells via a type IV secretion system, leads to cellular changes such as morphology, apoptosis, proliferation and cell motility, and stimulates gastric carcinogenesis. We investigated the effects of cytotoxin-associated gene A (CagA) and gastrokine 1 (GKN1) on cell proliferation, apoptosis, reactive oxygen species (ROS) production, epithelial-mesenchymal transition (EMT) and cell migration in CagA- or GKN1-transfected gastric epithelial cells and mucosal tissues from humans and mice infected with H.pylori. On the molecular level, H.pylori CagA induced increased cell proliferation, ROS production, antiapoptotic activity, cell migration and invasion. Moreover, CagA induced activation of NF-κB and PI3K/Akt signaling pathways and EMT-related proteins. In addition, H.pylori CagA reduced GKN1 gene copy number and expression in gastric cells and mucosal tissues of humans and mice. However, GKN1 overexpression successfully suppressed the carcinogenic effects of CagA through binding to CagA. These results suggest that GKN1 might be a target to inhibit the effects from H.pylori 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.