ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2013
Strain-specific suppression of microRNA-320 by carcinogenic Helicobacter pylori promotes expression of the antiapoptotic protein Mcl-1.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- Exploring the Shared miRNA-mRNA Signature Network Between Helicobacter pylori Infection and Gastric Cancer: A Comparative Study.Current microbiology · 2025Article
- Non-coding RNAs in bladder cancer, a bridge between gut microbiota and host?Frontiers in immunology · 2024Review
- Comprehensive insight into altered host cell-signaling cascades upon Helicobacter pylori and Epstein-Barr virus infections in cancer.Archives of microbiology · 2023Review
- miR-21 Targets ASPP2 to Inhibit Apoptosis via CHOP-Mediated Signaling inJournal of oncology · 2023Article
- miRNA-320 inhibits colitis-associated colorectal cancer by regulating the IL-6R/STAT3 pathway in mice.Journal of gastrointestinal oncology · 2022Article
- Bacteria-Mediated Oncogenesis and the Underlying Molecular Intricacies: What We Know So Far.Frontiers in oncology · 2022Review
- Review
- Metal homeostasis in pathogenic Epsilonproteobacteria: mechanisms of acquisition, efflux, and regulation.Metallomics : integrated biometal science · 2021Review
- Function of Non-coding RNA inFrontiers in molecular biosciences · 2021Review
- Mycoplasma hyopneumoniae J elicits an antioxidant response and decreases the expression of ciliary genes in infected swine epithelial cells.Scientific reports · 2020Article
- Whole genome sequencing inAnnals of translational medicine · 2019Article
- Multifaceted Roles of microRNAs in Host-Bacterial Pathogen Interaction.Microbiology spectrum · 2019Review
- The impacts of H. pylori virulence factors on the development of gastroduodenal diseases.Journal of biomedical science · 2018Review
- New insights ofWorld journal of clinical cases · 2018Review
- PlasmaInternational journal of clinical and experimental pathology · 2017Article
- miR-320 inhibited ovarian cancer oncogenicity via targeting TWIST1 expression.American journal of translational research · 2017Article
- Wnt/β-catenin, an oncogenic pathway targeted by H. pylori in gastric carcinogenesis.Oncotarget · 2015Review
- Dysregulation of non-coding RNAs in gastric cancer.World journal of gastroenterology · 2015Review
- Helicobacter pylori and microRNAs: Relation with innate immunity and progression of preneoplastic conditions.World journal of clinical oncology · 2015Review
- MicroRNA-23a enhances migration and invasion through PTEN in osteosarcoma.Cancer gene therapy · 2015Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Helicobacter pylori is the strongest risk factor for gastric cancer, and strains harboring the cag pathogenicity island, which translocates the oncoprotein CagA into host cells, further augment cancer risk. We previously reported that in vivo adaptation of a noncarcinogenic H. pylori strain (B128) generated a derivative strain (7.13) with the ability to induce adenocarcinoma, providing a unique opportunity to define mechanisms that mediate gastric carcinogenesis. MicroRNAs (miRNAs) are small noncoding RNAs that regulate expression of oncogenes or tumor suppressors and are frequently dysregulated in carcinogenesis. To identify miRNAs and their targets involved in H. pylori-mediated carcinogenesis, miRNA microarrays were performed on RNA isolated from gastric epithelial cells cocultured with H. pylori strains B128, 7.13, or a 7.13 cagA(-) isogenic mutant. Among 61 miRNAs differentially expressed in a cagA-dependent manner, the tumor suppressor miR-320 was significantly downregulated by strain 7.13. Since miR-320 negatively regulates the antiapoptotic protein Mcl-1, we demonstrated that H. pylori significantly induced Mcl-1 expression in a cagA-dependent manner and that suppression of Mcl-1 results in increased apoptosis. To extend these results, mice were challenged with H. pylori strain 7.13 or its cagA(-) mutant; consistent with cell culture data, H. pylori induced Mcl-1 expression in a cagA-dependent manner. In human subjects, cag(+) strains induced significantly higher levels of Mcl-1 than cag(-) strains, and Mcl-1 expression levels paralleled the severity of neoplastic lesions. Collectively, these results indicate that H. pylori suppresses miR-320, upregulates Mcl-1, and decreases apoptosis in a cagA-dependent manner, which likely confers an increased risk for gastric carcinogenesis.
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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.