ArticleOncogene2018
Helicobacter pylori infection promotes Aquaporin 3 expression via the ROS-HIF-1α-AQP3-ROS loop in stomach mucosa: a potential novel mechanism for cancer pathogenesis.
Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 68 citations in OpenAlex.
- The Multifunctional Roles of Aquaporins in Tumors: Focusing on Metabolism, Migration, and Regulation of the Tumor Microenvironment.International journal of molecular sciences · 2026Review
- Hypoxia-inducible factor-1α exacerbates immune injury induced by influenza A virus and Streptococcus pneumoniae coinfection.BMC infectious diseases · 2025Article
- VASN drives gastric tumorigenesis via activation of the COL4A1/PI3K/AKT axis during Helicobacter pylori infection.British journal of cancer · 2025Article
- STING contributes to the inflammation and proliferation ofInfection and immunity · 2025Article
- Hypoxia and Hypoxia-Reoxygenation Potentiate Helicobacter pylori Infection and Gastric Epithelial Cell Proliferation.Cancer medicine · 2025Article
- Article
- Genome-Wide Association Study to Identify Genetic Factors Linked to HBV Reactivation Following Liver Transplantation in HBV-Infected Patients.International journal of molecular sciences · 2024Article
- MOMASTAntioxidants (Basel, Switzerland) · 2024Article
- Article
- Peroxiporins and Oxidative Stress: Promising Targets to Tackle Inflammation and Cancer.International journal of molecular sciences · 2024Review
- PPAR-γ/NF-kB/AQP3 axis in M2 macrophage orchestrates lung adenocarcinoma progression by upregulating IL-6.Cell death & disease · 2024Article
- N6-methyladenosine modification of hypoxia-inducible factor-1α regulatesWorld journal of gastrointestinal oncology · 2024Article
- Review
- Review
- Gut microbes involvement in gastrointestinal cancers through redox regulation.Gut pathogens · 2023Review
- Comprehensive insight into altered host cell-signaling cascades upon Helicobacter pylori and Epstein-Barr virus infections in cancer.Archives of microbiology · 2023Review
- Aquaporins in Glandular Secretion.Advances in experimental medicine and biology · 2023Article
- Succinylation Inhibits the Enzymatic Hydrolysis of the Extracellular Matrix Protein Fibrillin 1 and Promotes Gastric Cancer Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Clinical value and molecular mechanism of AQGPs in different tumors.Medical oncology (Northwood, London, England) · 2022Review
- Siah2-GRP78 interaction regulates ROS and provides a proliferative advantage to Helicobacter pylori-infected gastric epithelial cancer cells.Cellular and molecular life sciences : CMLS · 2022Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori (H. pylori) is the major stomach carcinogen, but the molecular mechanism responsible for the pathogenesis of cancer development mediated by H. pylori infection is still unclear. Aquaporin 3 (AQP3), overexpressed in gastric carcinoma, has a crucial role in gastric carcinogenesis and progression. However, the triggers and precise regulations for AQP3 upregulation during gastric carcinogens also remain unknown. Here we report that H. pylori infection-mediated carcinogenesis may be mechanistically depended on the upregulation of AQP3 expression via reactive oxygen species (ROS) pathway activation in the stomach. The retrospective analyses of clinical samples from patients with gastric carcinoma and other different stages of gastric diseases indicated that AQP3 expression was positively associated with gastric mucosal disease progression and H. pylori infection status as well. Furthermore, H. pylori infection significantly upregulated AQP3 and HIF-1α expression and increased ROS amount in human gastric epithelial AGS and GES-1 cells. Blockage of ROS with inhibitors, NAC and DPI, markedly decreased the expression of AQP3 and HIF-1α in both AGS and GES-1 cells simultaneously. Furthermore, the increased AQP3 in cells was mechanistically due to the transcriptional regulation by HIF-1α. In addition, H. pylori infection exerted production of proinflammatory cytokines IL-6, IL-8, and TNF depending on AQP3 level. Importantly, these in vitro novel findings were further investigated in vivo in a mouse H. pylori infectious model. Our current studies identify the mechanistic link between H. pylori infection and AQP3 upregulation in the pathogenesis of gastric carcinoma, which involves the activation of the ROS-HIF-1α axis and the exacerbated ROS-HIF-1α-AQP3-ROS loop.
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