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Background <p>Glioblastoma (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.</p> Methods <p>Glioblastoma 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.</p> Results <p>TLR7 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.</p> Conclusion <p>TLR7 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.</p>

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TLR7 modulates glioblastoma progression through PI3K/AKT/mTOR pathway and immune microenvironment remodeling

  • 期刊论文

  • 发表日期：

    2025年12月13日

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  • Liwen Guo,
  • Xianlei Zhou,
  • Zhi Zhang,
  • Xuemei Zhang

摘要

Background

Glioblastoma (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.

Methods

Glioblastoma 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.

Results

TLR7 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.

Conclusion

TLR7 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.