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Tumour-Derived Extracellular Vesicles Containing dsRNA Induce Degradation of Ribosomal Protein mRNA in Platelets.

Created on 10 Aug 2026

Authors

Gaoge Sun, Yuhuan Tao, Zihan Liu, Kaixiang Zhang, Shuai Zuo, Shanwen Chen, Shufang Ning, Tianyi Zhang, Pengyuan Wang, Ying Zhang, Zhi John Lu, Hang Hubert Yin

Published in

Journal of extracellular vesicles. Volume 15. Issue 8. Pages e70339.

Abstract

Extracellular vesicles (EVs) mediate intercellular communication within the tumour microenvironment by carrying cargoes from paracrine parent cells. EVs have attracted great research interest for their ability to carry nucleic acids into recipient cells and modulate cellular functions. However, previous studies have largely focused on RNA sequence information rather than RNA structure features. Here, we observed that EVs derived from colorectal cancer cells are enriched with endogenous double‑stranded RNA (dsRNA), a danger‑associated molecular pattern (DAMP) that leads to the activation of dsRNA‑sensing pathways in recipient cells. Crucially, we investigated the specific crosstalk between tumour-derived EVs and circulating platelets. As anucleate cells, platelets are uniquely suited models for isolating the effects of exogenous nucleic acids. Our analysis reveals that endogenous dsRNA from tumour EVs activates the platelet OAS-RNASEL innate immune ribonuclease cascade and the RNASEL/ABCE1/PELO axis, resulting in the decay of ribosomal protein mRNAs. This study, spanning from clinical observation to mechanistic validation, uncovers a novel pathway of tumour-platelet communication. We identify EV-enriched endogenous dsRNA as a functional mediator that enables tumour cells to directly reprogram platelet transcriptomes, revealing a new dimension of tumour-immune modulation.

PMID:
42572919
Bibliographic data and abstract were imported from PubMed on 10 Aug 2026.

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