ArticlePloS one2013
Gli1 deletion prevents Helicobacter-induced gastric metaplasia and expansion of myeloid cell subsets.
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 52 papers.
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Who cites it
52 citing papers in PubMed, 69 citations in OpenAlex.
- Recent advances in spasmolytic polypeptide expressing metaplasia research.World journal of gastrointestinal oncology · 2026Review
- Roles of interleukins in spasmolytic polypeptide‑expressing metaplasia (Review).International journal of oncology · 2026Review
- Transcriptomic profiling reveals the role of Hedgehog signaling as a biomarker and in the pathogenesis of Ménétrier's disease.The Journal of pathology · 2026Article
- Myeloid-derived suppressor cells modulation in the context of tumor microenvironment for gastric cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Luteolin improves precancerous conditions of the gastric mucosa by binding STAT3 and inhibiting LCN2 expression.International journal of biological sciences · 2025Article
- Positive GLI1/INHBA feedback loop drives tumor progression in gastric cancer.Cancer science · 2024Article
- Role of Helicobacter pylori virulence factors and alteration of the Tumor Immune Microenvironment: challenges and opportunities for Cancer Immunotherapy.Archives of microbiology · 2024Review
- DDS Profile: Juanita L. Merchant, MD, PhD.Digestive diseases and sciences · 2023Article
- The Cxcr2Frontiers in immunology · 2023Article
- Schlafen4Frontiers in immunology · 2023Article
- The immune microenvironment in gastric adenocarcinoma.Nature reviews. Gastroenterology & hepatology · 2022Review
- GM-CSF is key in the efficacy of vaccine-induced reduction of Helicobacter pylori infection.Helicobacter · 2022Article
- Protocol for generating a mouse model of gastric MALT lymphoma and the identification of MALT lymphoma cell populations by immunostaining.STAR protocols · 2022Article
- Schlafens Can Put Viruses to Sleep.Viruses · 2022Review
- Effects ofFrontiers in immunology · 2022Review
- Schlafen family is a prognostic biomarker and corresponds with immune infiltration in gastric cancer.Frontiers in immunology · 2022Article
- Plasmacytoid Dendritic Cell-Derived Type I Interferon Is Involved in Helicobacter pylori Infection-Induced Differentiation of Schlafen 4-Expressing Myeloid-Derived Suppressor Cells.Infection and immunity · 2021Article
- The TLR4-TRIF-type 1 IFN-IFN-γ pathway is crucial for gastric MALT lymphoma formation afteriScience · 2021Article
- Review
- Stomach-specific c-Myc overexpression drives gastric adenoma in mice through AKT/mammalian target of rapamycin signaling.Bosnian journal of basic medical sciences · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic inflammation in the stomach induces metaplasia, the pre-cancerous lesion that precedes inflammation-driven neoplastic transformation. While Hedgehog signaling contributes to the initiation of some cancers, its role in gastric transformation remains poorly defined. We found that Helicobacter-infected C57BL/6 mice develop extensive mucous cell metaplasia at 6 month but not at 2 months post-infection. Gastric metaplasia coincided with the appearance of CD45(+)MHCII(+)CD11b(+)CD11c(+) myeloid cells that were normally not present in the chronic gastritis at 2 months. The myeloid regulatory gene Schlafen-4 was identified in a microarray analysis comparing infected WT versus Gli1 null mice and was expressed in the CD11b(+)CD11c(+) myeloid population. Moreover this same population expressed IL-1β and TNFα pro-inflammatory cytokines. By 6 months, the mucous neck cell metaplasia (SPEM) expressed IL-6, phosphorylated STAT3 and the proliferative marker Ki67. Expression was not observed in Gli1 mutant mice consistent with the requirement of Gli1 to induce this pre-neoplastic phenotype. Ectopic Shh ligand expression alone was not sufficient to induce SPEM, but with Helicobacter infection synergistically increased the histologic severity observed with the inflammation. Therefore Hedgehog signaling is required, but is not sufficient to generate pre-neoplastic changes during chronic gastritis. Gli1-dependent myeloid cell differentiation plays a pivotal role in the appearance of myeloid cell subtypes ostensibly required for SPEM development. Moreover, it suggests that therapies capable of targeting this phenotypic switch might prevent progression to metaplasia, the pre-neoplastic change that develops prior to dysplasia and gastric cancer, which also occurs in other epithelial-derived neoplasias initiated by chronic inflammation.
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