ArticleCell death & disease2023
Glioma-derived LRIG3 interacts with NETO2 in tumor-associated macrophages to modulate microenvironment and suppress tumor growth.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Article
- LRIG2 suppresses NK cell-induced GSDME-mediated pyroptosis via the LAMP1-STAT3 pathway in glioma.Journal for immunotherapy of cancer · 2026Article
- MET-mediated phosphorylation of YANK2 at Y282 inhibits NEDD4L-dependent SUMOylation and degradation, promoting chemoresistance in glioblastoma.Molecular biomedicine · 2026Article
- Identifying Potential Diagnostic and Therapeutic Targets for Infantile Hemangioma Using WGCNA and Machine Learning Algorithms.Biochemical genetics · 2025Article
- Exploring the regulatory role of CNPY3 as a prognostic biomarker on human glioma cell migration, invasion and immune infiltration.Cancer biomarkers : section A of Disease markers · 2025Article
- The two-sided battlefield of tumour-associated macrophages in glioblastoma: unravelling their therapeutic potential.Discover oncology · 2024Review
- Co-culture models for investigating cellular crosstalk in the glioma microenvironment.Cancer pathogenesis and therapy · 2024Review
- GPR65 contributes to constructing immunosuppressive microenvironment in glioma.Neurosurgical review · 2024Article
- YANK2 activated by Fyn promotes glioma tumorigenesis via the mTOR-independent p70S6K activation pathway.Scientific reports · 2024Article
- CD58 acts as a tumor promotor in hepatocellular carcinoma via activating the AKT/GSK-3β/β-catenin pathway.Journal of translational medicine · 2023Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor-associated macrophages (TAMs) account for 30-50% of glioma microenvironment. The interaction between glioma tumor cells and TAMs can promote tumor progression, but the intrinsic mechanisms remain unclear. Herein, we reported that soluble LRIG3 (sLRIG3) derived from glioma tumor cells can block the M2 polarization of TAMs via interacting with NETO2, thus suppressing GBM malignant progression. The expression or activity of ADAM17 in glioma cells was positively correlated with the expression of sLRIG3 in cell supernatant. Soluble LRIG3 can suppress the M2-like polarity transformation of TAMs and inhibit the growth of tumor. High expression of LRIG3 predicts a good prognosis in patients with glioma. Mass spectrometry and Co-immunoprecipitation showed that sLRIG3 interacts with the CUB1 domain of NETO2 in TAMs. Silencing or knockout of NETO2 could block the effect of sLRIG3, which inhibited the M2-like polarity transformation of TAMs and promoted GBM tumor growth. However, overexpressing His-target NETO2 with CUB1 deletion mutation does not fully recover the suppressive effects of sLRIG3 on the TAM M2-polarization in NETO2-Knockout TAMs. Our study revealed vital molecular crosstalk between GBM tumor cells and TAMs. Glioma cells mediated the M2 polarization of TAM through the sLRIG3-NETO2 pathway and inhibited the progression of GBM, suggesting that sLRIG3-NETO2 may be a potential target for GBM treatment.
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