ArticleOncotarget2016
IL-10 secreted by M2 macrophage promoted tumorigenesis through interaction with JAK2 in glioma.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed, 126 citations in OpenAlex.
- Remodeling the Immune Landscape: How Obesity-Induced SASPs Create a Pro-Tumorigenic Niche.Current obesity reports · 2026Review
- Resiquimod-loaded magnetic nanoparticles reprogram macrophages and induce oxidative cytotoxicity against triple-negative breast cancer cells.International journal of pharmaceutics: X · 2026Article
- Y-box binding protein-1 at the crossroads of DNA damage response and tumor immune evasion.JNCI cancer spectrum · 2026Review
- CCAAT/enhancer-binding protein delta regulates miRs-4257 and 3156 to attenuate the interleukin 12 through small extracellular vesicle transmission in glioblastoma.Cancer cell international · 2026Article
- Tetrabenazine-induced miR-34a-5p suppresses the tumorigenicity of radioresistant colorectal cancer by inhibiting M2 macrophage polarization.Cell communication and signaling : CCS · 2025Article
- Nucleic acid-based delivery system delivering platinum drugs cooperates with siRNA for potentiated chemo-immunotherapy by reducing phosphatidylserine exposure and activating the cGAS-STING pathway.Acta pharmaceutica Sinica. B · 2025Article
- Immune factors and their role in tumor aggressiveness in glioblastoma: Atypical cadherin FAT1 as a promising target for combating immune evasion.Cellular & molecular biology letters · 2025Review
- Gpr109A in TAMs promoted hepatocellular carcinoma via increasing PKA/PPARγ/MerTK/IL-10/TGFβ induced M2c polarization.Scientific reports · 2025Article
- Immunophenotypic Profile of Adult Glioblastoma IDH-Wildtype Microenvironment: A Cohort Study.Cancers · 2024Article
- Unveiling the Inflammatory Landscape of Recurrent Glioblastoma through Histological-Based Assessments.Cancers · 2024Review
- Role for BLT1 in regulating inflammation within adipose tissue immune cells of aged mice.Immunity & ageing : I & A · 2024Article
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- The Streptococcus virulence protein PepO triggers anti-tumor immune responses by reprograming tumor-associated macrophages in a mouse triple negative breast cancer model.Cell & bioscience · 2023Article
- TGF-β in correlation with tumor progression, immunosuppression and targeted therapy in colorectal cancer.Medical oncology (Northwood, London, England) · 2023Review
- Drug metabolism-related gene ABCA1 augments temozolomide chemoresistance and immune infiltration abundance of M2 macrophages in glioma.European journal of medical research · 2023Article
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- The Importance of M1-and M2-Polarized Macrophages in Glioma and as Potential Treatment Targets.Brain sciences · 2023Review
- The Putative S1PR1 Modulator ACT-209905 Impairs Growth and Migration of Glioblastoma Cells In Vitro.Cancers · 2023Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
M2 tumor-associated macrophage has been found to play a supportive role in the progression of glioma. The underlying mechanism, nevertheless, has been largely unknown. In our study, to investigate how M2 macrophage played role in glioma, firstly we've analyzed the clinicopathological significance of M2 macrophage existence on clinical tissues of glioma using detection of CD163 expression with immunohistochemistry. Then, we've artificially induced M2 macrophage from human monocyte cell line THP-1, followed by co-culture with glioma cell lines in vitro. It was found that M2 macrophage was shown to be markedly distributed in glioma relative to paired normal control; and high prevalence of M2 macrophage was significantly associated with poorer overall survival and tumor progression. Moreover, M2 macrophage was found to be able to promote the growth in vitro and tumorigenesis in vivo in xenografted mice model. Mechanistically, it is IL-10 from M2 macrophage that was shown to promote proliferation, dependent on activation of JAK2/STAT3 pathway. Further, IL-10 was found to be able to interact with JAK2 in glioma cells. Taking together, we for the first time found that IL-10 from M2 macrophage promoted proliferation of glioma through interaction with JAK2; thereby activating the JAK2/STAT3 pathway, indicative of IL-10 could be used as a therapeutic target in the curing of glioma.
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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.