ArticleYonsei medical journal2016
Activation of NF-κB and AP-1 Mediates Hyperproliferation by Inducing β-Catenin and c-Myc in Helicobacter pylori-Infected Gastric Epithelial Cells.
Article in Yonsei medical journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 26 citations in OpenAlex.
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- Integrated single-cell RNA sequencing reveals the tumor heterogeneity and microenvironment landscape during liver metastasis in adenocarcinoma of esophagogastric junction.Frontiers in immunology · 2024Article
- Nickel oxide nanoparticles exposure as a risk factor for male infertility: "Frontiers in endocrinology · 2023Article
- Linking dysbiosis to precancerous stomach through inflammation: Deeper than and beyond imaging.Frontiers in immunology · 2023Review
- Helicobacter Pylori and Gastric Cancer Progression.Current microbiology · 2022Review
- RacGAP1 promotes the malignant progression of cervical cancer by regulating AP-1 via miR-192 and p-JNK.Cell death & disease · 2022Article
- Kinases and therapeutics in pathogen mediated gastric cancer.Molecular biology reports · 2022Review
- The Role and Interactions of Programmed Cell Death 4 and its Regulation by microRNA in Transformed Cells of the Gastrointestinal Tract.Frontiers in oncology · 2022Review
- Inflammation-Induced Tumorigenesis and Metastasis.International journal of molecular sciences · 2021Review
- Astaxanthin InhibitsJournal of cancer prevention · 2020Article
- Advance on toxicity of metal nickel nanoparticles.Environmental geochemistry and health · 2020Review
- The Complex Network between MYC Oncogene and microRNAs in Gastric Cancer: An Overview.International journal of molecular sciences · 2020Review
- The NF-κB Signaling Pathway, the Microbiota, and Gastrointestinal Tumorigenesis: Recent Advances.Frontiers in immunology · 2020Review
- β-carotene Inhibits Expression of c-Myc and Cyclin E inJournal of cancer prevention · 2019Article
- Lipopolysaccharide stimulates endogenous β-glucuronidase via PKC/NF-κB/c-myc signaling cascade: a possible factor in hepatolithiasis formation.Molecular and cellular biochemistry · 2018Article
- Overexpression of MYC binding protein promotes invasion and migration in gastric cancer.Oncology letters · 2018Article
- Role of microRNAs and Exosomes inFrontiers in microbiology · 2018Review
- Role of Δ133p53 isoform in NF-κB inhibitor PDTC-mediated growth inhibition of MKN45 gastric cancer cells.World journal of gastroenterology · 2017Article
- CDK5 functions as a tumor promoter in human colorectal cancer via modulating the ERK5-AP-1 axis.Cell death & disease · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeIn the gastric mucosa of Helicobacter pylori (H. pylori)-infected patients with gastritis or adenocarcinoma, proliferation of gastric epithelial cells is increased. Hyperproliferation is related to induction of oncogenes, such as β-catenin and c-myc. Even though transcription factors NF-κB and AP-1 are activated in H. pylori-infected cells, whether NF-κB or AP-1 regulates the expression of β-catenein or c-myc in H. pylori-infected cells has not been clarified. The present study was undertaken to investigate whether H. pylori-induced activation of NF-κB and AP-1 mediates the expression of oncogenes and hyperproliferation of gastric epithelial cells. MATERIALS AND
methodsGastric epithelial AGS cells were transiently transfected with mutant genes for IκBα (MAD3) and c-Jun (TAM67) or treated with a specific NF-κB inhibitor caffeic acid phenethyl ester (CAPE) or a selective AP-1 inhibitor SR-11302 to suppress activation of NF-κB or AP-1, respecively. As reference cells, the control vector pcDNA was transfected to the cells. Wild-type cells or transfected cells were cultured with or without H. pylori.
resultsH. pylori induced activation of NF-κB and AP-1, cell proliferation, and expression of oncogenes (β-catenein, c-myc) in AGS cells, which was inhibited by transfection of MAD3 and TAM67. Wild-type cells and the cells transfected with pcDNA showed similar activities of NF-κB and AP-1, proliferation, and oncogene expression regardless of treatment with H. pylori. Both CAPE and SR-11302 inhibited cell proliferation and expression of oncogenes in H. pylori-infected cells.
conclusionH. pylori-induced activation of NF-κB and AP-1 regulates transcription of oncogenes and mediates hyperproliferation in gastric epithelial cells.
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