ArticleOncogene2013
Rebamipide abolishes Helicobacter pylori CagA-induced phospholipase D1 expression via inhibition of NFκB and suppresses invasion of gastric cancer cells.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 48 citations in OpenAlex.
- The Reg gene family: roles in gastric and colorectal cancer progression and its potential for targeted therapy.Discover oncology · 2025Review
- PLD1 is a key player in cancer stemness and chemoresistance: Therapeutic targeting of cross-talk between the PI3K/Akt and Wnt/β-catenin pathways.Experimental & molecular medicine · 2024Review
- Shaoyao Decoction reduced T lymphocyte activation by regulating of intestinal flora and 5-hydroxytryptamine metabolism in ulcerative colitis.Chinese medicine · 2024Article
- A review of signal pathway induced by virulent protein CagA ofFrontiers in cellular and infection microbiology · 2023Review
- Hypoxia-induced cofilin 1 promotes hepatocellular carcinoma progression by regulating the PLD1/AKT pathway.Clinical and translational medicine · 2021Article
- Identification and validation of critical alternative splicing events and splicing factors in gastric cancer progression.Journal of cellular and molecular medicine · 2020Article
- Treatment with Gold Nanoparticles UsingInternational journal of molecular sciences · 2020Article
- Integrated Analyses Identify Immune-Related Signature Associated with Qingyihuaji Formula for Treatment of Pancreatic Ductal Adenocarcinoma Using Network Pharmacology and Weighted Gene Co-Expression Network.Journal of immunology research · 2020Article
- HP-CagA+ Regulates the Expression of CDK4/CyclinD1 viaInternational journal of molecular sciences · 2019Article
- Tissue microarray staining reveals PLD1 and Sp1 have a collaborative, pro-tumoral effect in patients with osteosarcomas.Oncotarget · 2017Article
- PLD1 overexpression promotes invasion and migration and function as a risk factor for Chinese glioma patients.Oncotarget · 2017Article
- Simultaneous high expression of PLD1 and Sp1 predicts a poor prognosis for pancreatic ductal adenocarcinoma patients.Oncotarget · 2016Article
- MiR-206 suppresses epithelial mesenchymal transition by targeting TGF-β signaling in estrogen receptor positive breast cancer cells.Oncotarget · 2016Article
- The Role ofGastroenterology research and practice · 2016Review
- MicroRNA-638 inhibits cell proliferation by targeting phospholipase D1 in human gastric carcinoma.Protein & cell · 2015Article
- AID, p53 and MLH1 expression in early gastric neoplasms and the correlation with the background mucosa.Oncology letters · 2015Article
- Helicobacter pylori virulence factor CagA promotes tumorigenesis of gastric cancer via multiple signaling pathways.Cell communication and signaling : CCS · 2015Review
- Nuclear factor kappa B role in inflammation associated gastrointestinal malignancies.World journal of gastroenterology · 2015Review
- Phospholipase D in cell signaling: from a myriad of cell functions to cancer growth and metastasis.The Journal of biological chemistry · 2014Review
- Cellular and physiological roles for phospholipase D1 in cancer.The Journal of biological chemistry · 2014Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infection with cagA-positive Helicobacter pylori is a risk factor for the development of severe gastritis and gastric cancer (GC). CagA protein is injected into gastric epithelial cells and deregulates a variety of cellular signaling molecules. Phospholipase D (PLD) is elevated in many different types of human cancers and has been implicated as a critical factor in inflammation and carcinogenesis. In this study, we show that infection with cagA-positive H. pylori in GC cells significantly induces PLD1 expression via CagA-dependent activation of nuclear factor κB (NFκB). Interestingly, the level of PLD1 protein and IκBα phosphorylation is aberrantly upregulated in H. pylori-infected human GC tissues. Infection with cagA-positive H. pylori and expression of CagA enhanced the binding of NFκB to the PLD1 promoter, and two functional NFκB-binding sites were identified within the PLD1 promoter. Rebamipide, a mucosal-protective antiulcer agent, abolished H. pylori cagA-induced PLD1 expression via inhibition of binding of NFκB to the PLD1 promoter, and also inhibited PLD activity. Moreover, rebamipide suppressed H. pylori-induced matrix metalloproteinase-9, interleukin-8 and activation-induced cytidine deaminase expression as well as invasion of GC cells through downregulation of PLD1. Our data suggest that H. pylori cagA targets PLD1 for invasion of GC cells, and rebamipide might contribute to the antitumorigenic effect of GC cells via inhibition of the H. pylori cagA-NFκB-PLD1 signaling pathway.
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