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Systemic Propagation of STING Signalling via Generation of Large Extracellular Vesicles.
Jiae Lee1,2, Annabel Vernon1, Hyung Joon Park1
1Department of Biochemistry, University of Washington, Seattle, Washington, USA.
Journal of Extracellular Vesicles
|May 10, 2026
Summary
Malignant cells release large extracellular vesicles (EVs) through a conserved STING pathway. This process drives tumor progression and triggers a systemic immune response, offering new therapeutic targets.
Area of Science:
- Oncology
- Immunology
- Cell Biology
Background:
- Large extracellular vesicles (EVs) from tumor cells are implicated in cancer progression.
- The precise mechanisms driving large EV biogenesis and their in vivo functions remain largely unknown.
Purpose of the Study:
- To investigate the mechanisms of large EV biogenesis in malignant cells.
- To explore the role of the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway in large EV production and anti-tumor immunity.
Main Methods:
- Utilized a Drosophila tumor model to study large EV biogenesis.
- Investigated the STING signaling pathway's involvement using genetic and cellular assays.
- Performed EV transplantation experiments in Drosophila larvae.
Main Results:
- Demonstrated that large EV biogenesis from malignant cells is evolutionarily conserved.
- Uncovered a critical role for the cGAS-STING pathway in driving large EV biogenesis.
- Showed that STING signaling, independent of TBK1/IKKβ, regulates EV production via JNK and FAK.
- Transplanted EVs induced a systemic immune response by activating STING in macrophage-like cells.
Conclusions:
- Established a novel Drosophila model for studying tumor-derived large EVs.
- Revealed a conserved mechanism linking STING signaling, EV biogenesis, and systemic anti-tumor immunity.
- Highlighted the STING pathway's role in propagating immune signals via EVs from tumor cells.
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