ArticleJournal of cellular and molecular medicine2021
NOD2 deficiency confers a pro-tumorigenic macrophage phenotype to promote lung adenocarcinoma progression.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
- Review
- Lung microbiota analysis in early-stage lung adenocarcinoma.Microbiology spectrum · 2026Article
- The TRIM-cancer paradox: BCG as a programmable vaccine platform and a mechanistic probe for rational immunotherapy design.Frontiers in immunology · 2026Review
- The Emerging Mechanisms and Therapeutic Potentials of Dendritic Cells in NSCLC.Journal of inflammation research · 2025Review
- Pyroptosis-associated genes and tumor immune response in endometrial cancer.Discover oncology · 2024Article
- Role and molecular mechanism of NOD2 in chronic non-communicable diseases.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Prognostic value of inflammation and immune-related gene NOD2 in clear cell renal cell carcinoma.Human cell · 2024Article
- The genomic landscape of the immune system in lung cancer: present insights and continuing investigations.Frontiers in genetics · 2024Review
- The GJB3 correlates with the prognosis, immune cell infiltration, and therapeutic responses in lung adenocarcinoma.Open medicine (Warsaw, Poland) · 2024Article
- Transcriptomic landscape based on annotated clinical features reveals PLPP2 involvement in lipid raft-mediated proliferation signature of early-stage lung adenocarcinoma.Journal of experimental & clinical cancer research : CR · 2023Article
- A novel necroptosis related gene signature and regulatory network for overall survival prediction in lung adenocarcinoma.Scientific reports · 2023Article
- STK11 mutation impacts CD1E expression to regulate the differentiation of macrophages in lung adenocarcinoma.Immunity, inflammation and disease · 2023Article
- LARRPM restricts lung adenocarcinoma progression and M2 macrophage polarization through epigenetically regulating LINC00240 and CSF1.Cellular & molecular biology letters · 2022Article
- Emerging role of RNA sensors in tumor microenvironment and immunotherapy.Journal of hematology & oncology · 2022Review
- Signature based on RNA-binding protein-related genes for predicting prognosis and guiding therapy in non-small cell lung cancer.Frontiers in genetics · 2022Article
- Development of a Risk Predictive Model for Evaluating Immune Infiltration Status in Invasive Thyroid Carcinoma.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- NOD2 deficiency confers a pro-tumorigenic macrophage phenotype to promote lung adenocarcinoma progression.Journal of cellular and molecular medicine · 2021Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nucleotide-binding and oligomerization domain-containing protein 2 (NOD2) was a member of the NOD-like receptor family and played an important role in the innate immune response. Dysregulated NOD2 had been reported to contribute to tumorigenesis and progression. Here, we investigated that decreased NOD2 expressions could affect the phenotypic polarization of tumour-associated macrophages and thus lead to the poor prognosis of lung adenocarcinoma patients. We clustered the patients by the single-sample gene set enrichment analysis of tumour microenvironment and 13 prognostic differentially expressed immune-related genes (PDEIRGs) were obtained based on prognostic analyses. After multiple assessments on the 13 PDEIRGs, NOD2 was considered to be the central immune gene and had a strong effect on suppressing tumour progression. Decreased NOD2 expression could be induced by cancer cells and lead to the phenotypic polarization of macrophages from protective M1 phenotype to pro-tumorigenic M2 subtype which might be attributed to the down-regulating of NF-κB signalling pathway. This study draw attention to the role of inhibited innate immune function mediated by depletion of NOD2 in the TME. Our work also points to a potential strategy of NOD2-mediated TAM-targeted immunotherapy.
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