ArticleScientific reports2025
PD-L1 autoregulation promotes the proliferation, migration and invasion of glioblastoma cells via GP130/JAK2/STAT3/IRAK2/IL6 signaling pathway.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Advances in the role of astrocytes in glioma progression and therapy.Acta pharmacologica Sinica · 2026Review
- Mechanisms of Therapeutic Resistance and Recent Advances in Glioblastoma Treatment.Immunology and cell biology · 2026Review
- p62/SQSTM1-TRAF6/RIP1 complexes activate NF-κB-mediated PD-L1 expression and promote T-cell apoptosis in MKN45 gastric cancer cells.Journal of gastrointestinal oncology · 2026Article
- Targeting EHMT2 inhibition in glioblastoma: effects on tumor progression and STAT3 signaling.Translational cancer research · 2026Article
- Decoding the tumor-aging axis: from bench to clinical.Frontiers in immunology · 2026Review
- Glioblastoma pathophysiology: roles of aging driven changes in STAT3 interactions with NF-κB dimer components in the modulation of the mitochondrial melatonergic pathway and night-time inflammation resolution.Exploration of targeted anti-tumor therapy · 2026Review
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Authors and funding
28 authors.
Funding
Abstract
Glioblastoma (GBM) cells mediate immunosuppressive microenvironment, leading to poor response to programmed death-ligand 1(PD-L1) inhibitor therapy. How PD-L1 in GBM cells confers to GBM immunosuppressive microenvironment remains unclear. Here, we demonstrate that PD-L1 activated GP130/JAK2/STAT3/IRAK2/NFκB/IL6 pathway. We showed that PD-L1 was elevated in human primary GBM and promoted GBM cell viability, migration and invasion via activating janus kinase 2(JAK2) by interacting with glycoprotein 130(GP130) and PD-1 in GBM cells, leading to the activation of signal transducer and activator of transcription 3 (STAT3), a master that renders GBM immunosuppression. Overexpressing STAT3 reversed the effect of silencing PD-L1-mediated cell viability, proliferation, migration and invasion. STAT3 promoted interleukin-1 receptor-associated kinase 2(IRAK2) transcription. IRAK2 overexpression rescued the effect of silencing STAT3-mediated cell viability, proliferation, migration and invasion. Additionally, IRAK2 facilitated interleukin-6 (IL6) expression via activating nuclear factor kappa-B (NFκB). Our results indicate that PD-L1/GP130/JAK2/STAT3/IRAK2/NFκB/IL6 axis promotes GBM cell viability, proliferation, migration and invasion via interacting with GP130 and PD-1 in GBM cells. Additionally, STAT3 transcriptionally promoted PD-L1 expression, thus forming loops to lead to PD-L1 autoregulation. IL6 positively correlated with GBM-associated macrophages, myeloid-derived suppressor cells and the inhibition of dendritic cells. Our study suggests that PD-L1 autoregulation may create immunosuppressive GBM via activating GP130/JAK2/STAT3/IRAK2/IL-6 pathway.
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