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Updated: Jun 20, 2026
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Paramyxoviruses for Tumor-targeted Immunomodulation: Design and Evaluation Ex Vivo
Published on: January 7, 2019
VEGFR2 inhibition potentiates STING-mediated antitumor immunity
Fangping Han1, Pengbo Sun2, Yuanyuan Wei1
1School of Pharmaceutical Sciences, State Key Laboratory of Membrane Biology, Tsinghua-Peking Center for Life Sciences, Beijing Frontier Research Center for Biological Structure, Tsinghua University, Beijing, China.
Cell Reports
|June 18, 2026
Summary
This study reveals that VEGFR2 negatively regulates STING immune signaling. Inhibiting VEGFR2 enhances STING activation, boosting antitumor immunity for potential cancer therapies.
Area of Science:
- Immunology
- Molecular Biology
- Cancer Research
Background:
- STING (stimulator of interferon genes) is crucial for innate and adaptive immunity, showing promise in cancer immunotherapy.
- Receptor tyrosine kinases (RTKs) are implicated in cancer, but their interaction with STING is not fully understood.
Purpose of the Study:
- To elucidate the regulatory relationship between STING and receptor tyrosine kinases.
- To investigate the potential of targeting this interaction for enhanced cancer immunotherapy.
Main Methods:
- Utilized cell-based assays to study the cGAMP-STING signaling pathway.
- Investigated the role of VEGFR2 and its inhibitor Ki8751 in modulating STING activation.
- Assessed the in vivo antitumor effects of co-targeting VEGFR2 and STING.
Main Results:
- Identified VEGFR2 as a negative regulator of cGAMP-STING signaling via the AKT1 pathway.
- Demonstrated a reciprocal inhibitory feedback loop between STING and VEGFR2.
- Showed that VEGFR2 inhibition by Ki8751 amplifies STING responses and enhances STING-dependent antitumor immunity in vivo.
Conclusions:
- Established the VEGFR2-STING regulatory axis, highlighting a novel mechanism in immune regulation.
- Provided a mechanistic basis for combining VEGFR2 inhibitors with STING agonists to improve cancer immunotherapy outcomes.
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