ArticleBMC gastroenterology2002
Effect of interlukin-1beta on proliferation of gastric epithelial cells in culture.
Article in BMC gastroenterology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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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Who cites it
13 citing papers in PubMed, 46 citations in OpenAlex.
- Paracrine activin B-NF-κB signaling shapes an inflammatory tumor microenvironment in gastric cancer via fibroblast reprogramming.Journal of experimental & clinical cancer research : CR · 2023Article
- IL-1β Promotes Expansion of IL-33American journal of respiratory cell and molecular biology · 2022Article
- The TNF-Alpha Inducing Protein is Associated With Gastric Inflammation and Hyperplasia in a Murine Model ofFrontiers in pharmacology · 2022Article
- Potential mechanisms of tumor progression associated with postoperative infectious complications.Cancer metastasis reviews · 2021Review
- Interleukin-1B signalling leads to increased survival of gastric carcinoma cells through a CREB-C/EBPβ-associated mechanism.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2016Article
- Osteopontin depletion decreases inflammation and gastric epithelial proliferation during Helicobacter pylori infection in mice.Laboratory investigation; a journal of technical methods and pathology · 2015Article
- NF-kappaB-dependent microRNA-425 upregulation promotes gastric cancer cell growth by targeting PTEN upon IL-1β induction.Molecular cancer · 2014Article
- Analysis of cell hyperplasia and parietal cell dysfunction induced by Ostertagia ostertagi infection.Veterinary research · 2013Article
- Roles of inflammatory cytokines in the progression of gastric cancer: friends or foes?Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2010Review
- TLR-independent induction of human monocyte IL-1 by phosphoglycolipids from thermophilic bacteria.Glycoconjugate journal · 2008Article
- Tip-alpha (hp0596 gene product) is a highly immunogenic Helicobacter pylori protein involved in colonization of mouse gastric mucosa.Current microbiology · 2008Article
- Effects of Helicobacter pylori infection on gastric epithelial cell kinetics in patients with chronic renal failure.World journal of gastroenterology · 2005Article
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Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHelicobacter pylori is the main risk factor for the development of non-cardia gastric cancer. Increased proliferation of the gastric mucosa is a feature of H. pylori infection. Mucosal interkeukin-1beta production is increased in H. pylori infection and IL-1beta genotypes associated with increased pro-inflammatory activity are risk factors for the development of gastric cancer. The effect of IL-1beta on gastric epithelial cell proliferation has been examined in this study.
methodsAGS cells were cultured with IL-1beta. DNA synthesis was assed by [3H]thymidine incorporation and total viable cell numbers by MTT assay.
resultsIL-1beta dose dependently increased DNA synthesis and cell numbers. The enhanced proliferation was blocked by interleukin-1 receptor antagonist. Addition of neutralising antibody to GM-CSF reduced IL-1beta-stimulated proliferation by 31 +/- 4 %. GM-CSF alone significantly stimulated proliferation. Addition or neutralisation of IL-8 had no effect on basal or IL-1beta-stimulated proliferation. The tyrosine kinase inhibitor genistein completely blocked IL-1beta-stimulated proliferation and inhibition of the extracellular signal related kinase pathway with PD 98059 inhibited IL-1beta stimulated proliferation by 58 +/- 5 %.
conclusionsIL-1beta stimulates proliferation in gastric epithelial cells. Autocrine stimulation by GM-CSF contributes to this proliferative response. Signalling via tyrosine kinase activity is essential to the mitogenic response to IL-1beta. The extracellular signal related kinase pathway is involved in, but not essential to downstream signalling. IL-1beta may contribute to the hyperproliferation seen in H. pylori- infected gastric mucosa, and be involved in the carcinogenic process.
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