ArticleIrish journal of medical science2026
TLR7 modulates glioblastoma progression through PI3K/AKT/mTOR pathway and immune microenvironment remodeling.
Article in Irish journal of medical science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Recent progress and therapeutic strategies in the treatment of cervical neuroendocrine neoplasms (Review).International journal of molecular medicine · 2026Review
- Focused ultrasound for cellular mechanoactivation and nanomedicine delivery in cancer.Biomedical microdevices · 2026Review
- Meningeal immunity and "Interstitial" therapy: a new paradigm for immunotherapy in glioblastoma.Frontiers in immunology · 2026Review
- The Interaction of PI3K/AKT/mTOR Pathway with the Tumor Microenvironment: A Dual Engine Driving Breast Cancer Progression and Reshaping Treatment Strategies.Cancer management and research · 2026Review
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Authors and funding
4 authors.
Funding
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Abstract
backgroundGlioblastoma (GBM) is an aggressive brain tumor, necessitating the identification of new therapeutic targets. Toll-like receptor 7 (TLR7), a key component of innate immunity, influences oncological processes, but its role in GBM is unclear. This study investigates the impact of TLR7 overexpression on GBM and its underlying mechanisms.
methodsGlioblastoma cell lines (U87 and U251) were transfected with a pcDNA-TLR7 plasmid to induce overexpression, verified by qRT-PCR. Proliferation was assessed using CCK-8 and colony formation assays. Migration and invasion were evaluated via Transwell and wound healing assays. Activation of the PI3K/AKT/mTOR signaling pathway was analyzed by Western blotting. Macrophage polarization was studied by exposing M0 macrophages to the TLR7 agonist R837, followed by qRT-PCR and cytokine quantification.
resultsTLR7 was successfully overexpressed in U87 and U251 cells. TLR7 overexpression significantly reduced GBM cell proliferation, colony formation, migration, and invasion. It suppressed the PI3K/AKT/mTOR signaling pathway. In the tumor microenvironment, TLR7 promoted M1 macrophage polarization, increasing M1 markers and pro-inflammatory cytokines while suppressing M2 markers.
conclusionTLR7 suppresses glioblastoma by inhibiting cell progression via the PI3K/AKT/mTOR signaling pathway and promoting an anti-tumoral immune microenvironment. These findings suggest the potential of TLR7 as a promising therapeutic target for GBM.
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