ArticleThe Journal of experimental medicine2020
Glioma stem-like cells evade interferon suppression through MBD3/NuRD complex-mediated STAT1 downregulation.
Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 57 citations in OpenAlex.
- MicroRNA-124-targeted recombinant Zika virus: a dual-functional and safe candidate for vaccination and oncolytic virotherapy.Journal of virology · 2026Article
- IDH1-R132H enhances oncolytic HSV-1 therapy by facilitating viral entry and immune activation in glioma.Nature communications · 2026Article
- Notch Overexpression Potentiates Interferon Signaling in Glioma Cells.Current issues in molecular biology · 2026Article
- Bridging MBD3 functions in developmental biology and glioma heterogeneity to immune remodeling with future perspectives.Frontiers in immunology · 2026Review
- Therapy-induced senescent glioblastoma cells sustain a procancer immune microenvironment by activating DDX58-mediated STAT1 signaling.Neuro-oncology · 2025Article
- Epigenetic Alterations in Glioblastoma Multiforme as Novel Therapeutic Targets: A Scoping Review.International journal of molecular sciences · 2025Article
- Elevated nonhomologous end-joining by AATF enables efficient DNA damage repair and therapeutic resistance in glioblastoma.Nature communications · 2025Article
- Conserved chromatin regulators control the transcriptional immune response to intracellular pathogens in Caenorhabditis elegans.PLoS genetics · 2025Article
- PHGDH activation fuels glioblastoma progression and radioresistance via serine synthesis pathway.Journal of experimental & clinical cancer research : CR · 2025Article
- FSD1 inhibits glioblastoma diffuse infiltration through restriction of HDAC6-mediated microtubule deacetylation.Science China. Life sciences · 2025Article
- Emerging roles of CircRNA-miRNA networks in cancer development and therapeutic response.Non-coding RNA research · 2025Review
- Going viral: targeting glioblastoma using oncolytic viruses.Immunotherapy advances · 2025Review
- Constitutive type-1 interferons signaling activity in malignant gliomas.Journal of neuro-oncology · 2024Article
- Article
- A bio-orthogonal linear ubiquitin probe identifies STAT3 as a direct substrate of OTULIN in glioblastoma.Nucleic acids research · 2023Article
- Harnessing type I interferon-mediated immunity to target malignant brain tumors.Frontiers in immunology · 2023Review
- SPI1-mediated MIR222HG transcription promotes proneural-to-mesenchymal transition of glioma stem cells and immunosuppressive polarization of macrophages.Theranostics · 2023Article
- How cancer cells make and respond to interferon-I.Trends in cancer · 2023Review
- SARS-CoV-2 hijacks cellular kinase CDK2 to promote viral RNA synthesis.Signal transduction and targeted therapy · 2022Article
- The roles of histone modifications in tumorigenesis and associated inhibitors in cancer therapy.Journal of the National Cancer Center · 2022Review
Corrections and comments
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Authors and funding
25 authors at 5 institutions in 2 countries.
Funding
Abstract
Type I interferons (IFNs) are known to mediate antineoplastic effects during tumor progression. Type I IFNs can be produced by multiple cell types in the tumor microenvironment; however, the molecular mechanisms by which tumor cells evade the inhibition of immune microenvironment remain unknown. Here we demonstrate that glioma stem-like cells (GSCs) evade type I IFN suppression through downregulation of STAT1 to initiate tumor growth under inhospitable conditions. The downregulation of STAT1 is mediated by MBD3, an epigenetic regulator. MBD3 is preferentially expressed in GSCs and recruits NuRD complex to STAT1 promoter to suppress STAT1 expression by histone deacetylation. Importantly, STAT1 overexpression or MBD3 depletion induces p21 transcription, resensitizes GSCs to IFN suppression, attenuates GSC tumor growth, and prolongs animal survival. Our findings demonstrate that inactivation of STAT1 signaling by MBD3/NuRD provides GSCs with a survival advantage to escape type I IFN suppression, suggesting that targeting MBD3 may represent a promising therapeutic opportunity to compromise GSC tumorigenic potential.
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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.