ArticleCancer biology & therapy2015
GATA-3 augmentation down-regulates Connexin43 in Helicobacter pylori associated gastric carcinogenesis.
Article in Cancer biology & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 32 citations in OpenAlex.
- Review
- New perspectives on gastric disorders: the relationship between innate lymphoid cells and microbes in the stomach.Cellular and molecular life sciences : CMLS · 2025Review
- The plasticity of epithelial cells and its potential in the induced differentiation of gastric cancer.Cell death discovery · 2024Review
- Current Knowledge about Gastric Microbiota with Special Emphasis onCurrent issues in molecular biology · 2024Review
- Bridging Chronic Inflammation and Digestive Cancer: The Critical Role of Innate Lymphoid Cells in Tumor Microenvironments.International journal of biological sciences · 2024Review
- Current study of pathogenetic mechanisms and therapeutics of chronic atrophic gastritis: a comprehensive review.Frontiers in cell and developmental biology · 2024Review
- The role of Gata3 in renin cell identity.American journal of physiology. Renal physiology · 2023Article
- The Roles of Innate Lymphoid Cells in the Gastric Mucosal Immunology and Oncogenesis of Gastric Cancer.International journal of molecular sciences · 2023Review
- Global knowledge mapping and emerging trends in research between spasmolytic polypeptide-expressing metaplasia and gastric carcinogenesis: A bibliometric analysis from 2002 to 2022.Frontiers in cellular and infection microbiology · 2022Article
- Article
- The Role of Gastric Mucosal Immunity in Gastric Diseases.Journal of immunology research · 2020Review
- How doesWorld journal of gastroenterology · 2019Review
- Prognostic value of the mRNA expression of gap junction α members in patients with gastric cancer.Oncology letters · 2019Article
- Helicobacter Pylori Induces GATA3-Dependent Chitinase 3 Like 1 (CHI3L1) Upregulation and Contributes to Vascular Endothelial Injuries.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Connexin 43 maintains tissue polarity and regulates mitotic spindle orientation in the breast epithelium.Journal of cell science · 2019Article
- Effects ofOncology letters · 2018Article
- PBX1 attributes as a determinant of connexin 32 downregulation inWorld journal of gastroenterology · 2017Article
- Low expression of GATA3 promotes cell proliferation and metastasis in gastric cancer.Cancer management and research · 2017Article
- Group 2 Innate Lymphoid Cells Are Involved in Skewed Type 2 Immunity of Gastric Diseases Induced byMediators of inflammation · 2017Article
- Molecular mechanisms of gastric cancer initiation and progression by Helicobacter pylori.Current opinion in infectious diseases · 2016Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori (H. pylori) is a risk factor of gastric carcinoma, and inflammation with H.pylori infection has widely been suggested to trigger gastric carcinogenesis through "inflammation-carcinoma chain" (non-atrophic gastritis (NAG) → chronic atrophic gastritis (CAG) → intestinal metaplasia (IM) → dysplasia (DYS) and gastric carcinoma (GC)). Connexin43 (Cx43) is a major constituent of gap junction in normal gastric mucosa (NGM) and it is continuously down-regulated from normal gastric mucosa to precancerous lesions or ultimate gastric carcinoma, which shows novel target against gastric carcinoma by preventing the Cx43 decline. Our previous studies demonstrated that H. pylori infection in gastric mucosa down-regulates Cx43 expression, but its mechanism remains unknown. The transcriptional factor, GATA binding protein 3 (GATA-3) is the key to regulate adaptive immune response, which possibly relates to inflammation toward malignant transformation. Here the substantial rising of GATA-3 was screened by transcriptional factor microarray along the developmental stages of H. pylori associated gastric carcinoma. Moreover, the increased GATA-3 and inhibited Cx43 were confirmed in clinical specimens, Mongolian gerbils and normal gastric epithelial cell line GES-1 with H. pylori infection. GATA-3 silencing generated the Cx43 restoration both in intermediate differentiation gastric cancer cells BGC-803 and in H. pylori infected GES-1 cells. Dual-luciferase reporter assay further revealed the GATA-3 as one of Cx43 down-regulators by directly binding to its promoters. Together, the incremental GATA-3 is found in H. pylori associated gastric carcinogenesis, which is responsible for Cx43 inhibition as well.
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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.