ArticleCancer research2006
Balance between polyoma enhancing activator 3 and activator protein 1 regulates Helicobacter pylori-stimulated matrix metalloproteinase 1 expression.
Article in Cancer research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Helicobacter pylori and gastritis: the role of extracellular matrix metalloproteases, their inhibitors, and the disintegrins and metalloproteases--a systematic literature review.Digestive diseases and sciences · 2013Pooled it
- Review
- The Comprehensive Analysis of Specific Proteins as Novel Biomarkers Involved in the Diagnosis and Progression of Gastric Cancer.International journal of molecular sciences · 2023Review
- Matrix Metalloproteinases inInternational journal of molecular sciences · 2022Review
- Molecular alterations of cancer cell and tumour microenvironment in metastatic gastric cancer.Oncogene · 2018Review
- Review
- Gastrin stimulates MMP-1 expression in gastric epithelial cells: putative role in gastric epithelial cell migration.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
- Outer membrane inflammatory protein A, a new virulence factor involved in the pathogenesis of Helicobacter pylori.Molecular biology reports · 2014Article
- Helicobacter pylori virulence and cancer pathogenesis.Future oncology (London, England) · 2014Review
- Role of the tumor microenvironment in the pathogenesis of gastric carcinoma.World journal of gastroenterology · 2014Review
- Virulence Factors of Helicobacter pylori: A Review.Clinical medicine insights. Gastroenterology · 2014Review
- The significance of virulence factors in Helicobacter pylori.Journal of digestive diseases · 2013Review
- Helicobacter pylori in gastric carcinogenesis: mechanisms.Gastroenterology clinics of North America · 2013Review
- Transcription factor complex AP-1 mediates inflammation initiated by Chlamydia pneumoniae infection.Cellular microbiology · 2013Article
- Article
- Constitutive K-RasG12D activation of ERK2 specifically regulates 3D invasion of human pancreatic cancer cells via MMP-1.Molecular cancer research : MCR · 2012Article
- Pathogenesis of Helicobacter pylori-Related Gastroduodenal Diseases from Molecular Epidemiological Studies.Gastroenterology research and practice · 2012Article
- PEA3/ETV4-related transcription factors coupled with active ERK signalling are associated with poor prognosis in gastric adenocarcinoma.British journal of cancer · 2011Article
- Mechanisms of disease: Helicobacter pylori virulence factors.Nature reviews. Gastroenterology & hepatology · 2010Review
- Helicobacter pylori and gastric cancer: factors that modulate disease risk.Clinical microbiology reviews · 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
6 authors at 4 institutions in 3 countries.
Funding
Abstract
Helicobacter pylori infection and elevated expression of tissue matrix metalloproteinase 1 (MMP-1) are both associated with gastric cancer. We investigated the regulation of MMP-1 expression during H. pylori infection. Real-time reverse transcription-PCR was used to examine mucosal MMP-1 mRNA levels in 55 patients with gastric cancers and 61 control patients. Increased MMP-1 mRNA levels in the gastric mucosa and epithelial cells were observed in H. pylori infections in which both the cag pathogenicity island (PAI) and outer inflammatory protein A (OipA) were expressed. The combined induction of c-fos, c-jun, and polyoma enhancing activator-3 (pea-3) by H. pylori caused maximal increase in MMP-1 expression. Activation of the MMP-1 promoter by H. pylori involved occupation of the activator protein 1 (AP-1) sites at -72 and -181 and, surprisingly, vacancy of the -88 PEA-3 site. Electrophoretic mobility shift, supershift, and chromatin immunoprecipitation assays showed increased binding of c-Fos and c-Jun to the -72 and -181 AP-1 sites during H. pylori infection. Importantly, during wild-type H. pylori infection, we detected increased PEA-3 binding to the -72AP-1 site and decreased PEA-3 binding to the -88 PEA-3 site. However, during infection with the cag PAI and oipA mutants, PEA-3 binding to the -88 site was detected. MMP-1 and pea-3 activities are increased in gastric cancers. Maximal activation of MMP-1 transcription requires the cag PAI and OipA, which regulate AP-1 and PEA-3 binding. Thus, cag PAI and OipA provide a possible link between bacterial virulence factors and important host factors related to disease 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.