ArticleOncogene2018
MiR-22 sustains NLRP3 expression and attenuates H. pylori-induced gastric carcinogenesis.
Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
95 citing papers in PubMed, 164 citations in OpenAlex.
- Hypoxia-induced HMGB1/NLRP3/Caspase-1 signaling axis enhances proliferation of oral squamous cell carcinoma.British journal of cancer · 2026Article
- [Molecular mechanisms of chronic gastric mucosal inflammation induced byZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026Review
- Interplay Among Endothelial Dysfunction, NLRP3 Pathway Activation, and microRNAs in the Pathogenesis of Preeclampsia.Diseases (Basel, Switzerland) · 2026Review
- Caspase-1 in cancer and inflammatory diseases: a potential therapeutic target.Apoptosis : an international journal on programmed cell death · 2026Review
- Histone demethylase KDM4B epigenetically controls NLRP3 expression to enhance inflammatory responses.EMBO molecular medicine · 2026Article
- De novo discovery of bicyclic cysteine-rich peptides targeting gasdermin D.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Review
- Gastrointestinal inflammation and cancer: viral and bacterial interplay.Gut microbes · 2025Review
- Nrf2-Keap1 Pathway and NLRP3 Inflammasome in Parkinson's Disease: Mechanistic Crosstalk and Therapeutic Implications.Molecular neurobiology · 2025Review
- Targeting pattern recognition receptors for cancer therapy: Mechanisms and strategies.Acta pharmaceutica Sinica. B · 2025Review
- Pyroptosis in gastric mucosal injury‑related diseases (Review).International journal of molecular medicine · 2025Review
- Microbiota-driven epigenetic modifications in gastrointestinal cancer: Implications for pathogenesis and therapeutic strategies.World journal of microbiology & biotechnology · 2025Review
- Pyroptosis and chemical classification of pyroptotic agents.Molecular diversity · 2025Review
- Role of inflammasomes in cancer immunity: mechanisms and therapeutic potential.Journal of experimental & clinical cancer research : CR · 2025Review
- The Role of the Tumor Microenvironment (TME) in Advancing Cancer Therapies: Immune System Interactions, Tumor-Infiltrating Lymphocytes (TILs), and the Role of Exosomes and Inflammasomes.International journal of molecular sciences · 2025Review
- Cell death in tumor microenvironment: an insight for exploiting novel therapeutic approaches.Cell death discovery · 2025Review
- NLRP3 inflammasome in health and disease (Review).International journal of molecular medicine · 2025Review
- The Association between the NLRP3 Inflammasome and Specific Long-Non Coding RNAs (lncRNAs) in Cancer; New Perspective and Summary of Recent Studies.Cell biochemistry and biophysics · 2025Review
- Nanomaterial-Driven Regulated Cell Death: Mechanistic Insights and Novel Strategies for Tumor Therapy.International journal of nanomedicine · 2025Review
- Pyroptosis-related lncRNAs are potential biomarkers for predicting prognoses and immune landscapes in patients with gastric adenocarcinoma.Discover oncology · 2024Article
35 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic inflammation is the primary cause of gastric cancer (GC). NLRP3, as an important inflammasome component, has crucial roles in initiating inflammation. However, the potential roles of NLRP3 in GC is unknown. Here, we show that NLRP3 expression is markedly upregulated in GC, which promotes NLRP3 inflammasome activation and interleukin-1β (IL-1β) secretion in macrophages. In addition, NLRP3 binds to cyclin-D1 (CCND1) promoter and promotes its transcription in gastric epithelial cells. Consequently, NLRP3 enhances epithelial cells proliferation and GC tumorigenesis. Furthermore, we identify miR-22, which is constitutively expressed in gastric mucosa, as a suppressor of NLRP3. MiR-22 directly targets NLRP3 and attenuates its oncogenic effects in vitro and in vivo. However, Helicobacter pylori (H. pylori) infection suppresses miR-22 expression, while enhances NLRP3 expression, and that triggers uncontrolled proliferation of epithelial cells and the emergence of GC. Thus, our research describes a mechanism by which miR-22 suppresses NLRP3 and maintains homeostasis of gastric microenvironments and suggests miR-22 as a potential target for the intervention of GC.
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Registered trials
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.