ArticlePloS one2013
Helicobacter pylori promotes the expression of Krüppel-like factor 5, a mediator of carcinogenesis, in vitro and in vivo.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 49 citations in OpenAlex.
- AURKA regulates LGR5 in response to Helicobacter Pylori infection by modulating its deubiquitination.Cell death and differentiation · 2026Article
- Enhanced COMP expression induced by Helicobacter pylori drives gastric cancer progression by NOTCH2/SMAD3 pathway.Journal of gastroenterology · 2026Article
- Helicobacter pylori-induced aberrant methylation of ID4 mediated by DNMT3B drives gastric cancer progression via DEC1-SHH signaling pathway.Cell death & disease · 2025Article
- Review
- SOX9 is regulated by AURKA in response to Helicobacter pylori infection via EIF4E-mediated cap-dependent translation.Cancer letters · 2024Article
- Article
- Downregulation of miR‑7 and miR‑153 is involved inInternational journal of oncology · 2023Article
- CDK1 bridges NF-κB and β-catenin signaling in response to H. pylori infection in gastric tumorigenesis.Cell reports · 2023Article
- Gastric Stem Cell Biology and Helicobacter pylori Infection.Current topics in microbiology and immunology · 2023Article
- Animal Models andJournal of clinical medicine · 2022Review
- Metal homeostasis in pathogenic Epsilonproteobacteria: mechanisms of acquisition, efflux, and regulation.Metallomics : integrated biometal science · 2021Review
- Silencing of miR490-3p by H. pylori activates DARPP-32 and induces resistance to gefitinib.Cancer letters · 2020Article
- UHMK1 promotes gastric cancer progression through reprogramming nucleotide metabolism.The EMBO journal · 2020Article
- Targeted mobilization of Lrig1Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- CarcinogenicMolecular & cellular proteomics : MCP · 2019Article
- MicroRNA-153 functions as a tumor suppressor in gastric cancer via targeting Kruppel-like factor 5.Experimental and therapeutic medicine · 2018Article
- Down-regulation of KLF5 in cancer-associated fibroblasts inhibit gastric cancer cells progression by CCL5/CCR5 axis.Cancer biology & therapy · 2017Article
- SP and KLF Transcription Factors in Digestive Physiology and Diseases.Gastroenterology · 2017Review
- Article
- Early Molecular Events in Murine Gastric Epithelial Cells Mediated by Helicobacter pylori CagA.Helicobacter · 2016Article
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Authors and funding
18 authors at 4 institutions in 1 country.
Funding
Abstract
Helicobacter pylori is the strongest known risk factor for the development of gastric adenocarcinoma. H. pylori expresses a repertoire of virulence factors that increase gastric cancer risk, including the cag pathogenicity island and the vacuolating cytotoxin (VacA). One host element that promotes carcinogenesis within the gastrointestinal tract is Krüppel-like factor 5 (KLF5), a transcription factor that mediates key cellular functions. To define the role of KLF5 within the context of H. pylori-induced inflammation and injury, human gastric epithelial cells were co-cultured with the wild-type cag(+) H. pylori strain 60190. KLF5 expression was significantly upregulated following co-culture with H. pylori, but increased expression was independent of the cag island or VacA. To translate these findings into an in vivo model, C57BL/6 mice were challenged with the wild-type rodent-adapted cag(+) H. pylori strain PMSS1 or a PMSS1 cagE(-) isogenic mutant. Similar to findings in vitro, KLF5 staining was significantly enhanced in gastric epithelium of H. pylori-infected compared to uninfected mice and this was independent of the cag island. Flow cytometry revealed that the majority of KLF5(+) cells also stained positively for the stem cell marker, Lrig1, and KLF5(+)/Lrig1(+) cells were significantly increased in H. pylori-infected versus uninfected tissue. To extend these results into the natural niche of this pathogen, levels of KLF5 expression were assessed in human gastric biopsies isolated from patients with or without premalignant lesions. Levels of KLF5 expression increased in parallel with advancing stages of neoplastic progression, being significantly elevated in gastritis, intestinal metaplasia, and dysplasia compared to normal gastric tissue. These results indicate that H. pylori induces expression of KLF5 in gastric epithelial cells in vitro and in vivo, and that the degree of KLF5 expression parallels the severity of premalignant lesions in human gastric carcinogenesis.
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