ArticleGut pathogens2023
CMTM3 protects the gastric epithelial cells from apoptosis and promotes IL-8 by stabilizing NEMO during Helicobacter pylori infection.
Article in Gut pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Helicobacter pylori-Induced Persistent IGF2BP1 Activation Promotes Ferroptosis Resistance in Gastric Tumorigenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Bioinformatics Analysis of Publicly Available Datasets and Validation in a Mouse Model of Myocardial Infarction Through Coronary Artery Ligation.Journal of inflammation research · 2026Article
- Disruption of the biorhythm in gastric epithelial cell triggers inflammation in Helicobacter pylori-associated gastritis by aberrantly regulating NFIL3 via CagA activated ERK-SP1 pathway.Cell communication and signaling : CCS · 2025Article
- CMTM6 promotes hepatocellular carcinoma invasion and metastasis and tumor-associated neutrophil immunoinfiltration through the Wnt/β-catenin pathway.European journal of medical research · 2024Article
- CMTM4 inhibits gastric tumorigenesis and metastasis.Journal of gastrointestinal oncology · 2024Article
- Review
- AUF1-mediated inhibition of autophagic lysosomal degradation contributes to CagA stability andGut microbesArticle
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundCKLF-like MARVEL transmembrane domain containing 3 (CMTM3) plays an important role in cancer development. Although Helicobacter pylori (H. pylori) infection is a main cause of gastric cancer, the function of CMTM3 during H. pylori infection remains unclear. CMTM3 expression levels in tissues from H. pylori-infected patients and cells co-cultured with H. pylori were analyzed. qRT-PCR and ELISA were used to investigate the effects of CMTM3 on interleukin 8 (IL-8) expression. Annexin V/propidium iodide staining was performed to evaluate the function of CMTM3 in the apoptosis of gastric epithelial cells. Proteomic analysis was performed to explore the underlying mechanism of CMTM3 during H. pylori infection. The interaction between CMTM3 and NEMO was determined via co-immunoprecipitation, HA-ubiquitin pull-down assay, and immunofluorescence.
resultsH. pylori induced a significant increase in CMTM3 expression. CMTM3 inhibited gastric mucosal epithelial cells from apoptosis and increased the expression level of IL-8 during H. pylori infection. KEGG pathway enrichment analysis revealed that differentially expressed proteins were involved in epithelial cell signaling in H. pylori infection. CMTM3 directly interacted with NEMO, which promoted protein stabilization by down-regulation of its ubiquitylation.
conclusionsCMTM3 reduces apoptosis and promotes IL-8 expression in the gastric epithelial cells by stabilizing NEMO during H. pylori infection. These findings characterize a new role for CMTM3 in host-pathogen interactions and provide novel insight into the molecular regulation of NEMO.
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