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Updated: Apr 3, 2026
Author Spotlight: Exploring the Mechanisms of MicroRNA Loading into Extracellular Vesicles in Cancer Progression
Published on: October 6, 2023
Extracellular vesicle-mediated transfer of processed and functional RNY5 RNA
Sudipto K Chakrabortty1, Ashwin Prakash1, Gal Nechooshtan1
1Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA.
Abstract:
Extracellular vesicles (EVs) have been proposed as a means to promote intercellular communication. We show that when human primary cells are exposed to cancer cell EVs, rapid cell death of the primary cells is observed, while cancer cells treated with primary or cancer cell EVs do not display this response. The active agents that trigger cell death are 29- to 31-nucleotide (nt) or 22- to 23-nt processed fragments of an 83-nt primary transcript of the human RNY5 gene that are highly likely to be formed within the EVs. Primary cells treated with either cancer cell EVs, deproteinized total RNA from either primary or cancer cell EVs, or synthetic versions of 31- and 23-nt fragments trigger rapid cell death in a dose-dependent manner. The transfer of processed RNY5 fragments through EVs may reflect a novel strategy used by cancer cells toward the establishment of a favorable microenvironment for their proliferation and invasion.
Insights
Cancer cells release extracellular vesicles (EVs) containing RNY5 gene fragments that induce rapid cell death in primary cells, suggesting a novel cancer communication strategy.
Area of Science:
- Molecular Biology
- Cell Biology
- Cancer Research
Background:
- Extracellular vesicles (EVs) mediate intercellular communication.
- Cancer cells interact with their surrounding microenvironment.
Purpose of the Study:
- To investigate the mechanism by which cancer cell EVs affect primary cells.
- To identify the active agents within EVs responsible for cellular responses.
Main Methods:
- Exposure of human primary cells to cancer cell EVs.
- Analysis of RNA fragments within EVs.
- Treatment of primary cells with purified RNA fragments and synthetic analogs.
Main Results:
- Cancer cell EVs induced rapid cell death in primary cells, but not vice versa.
- 29-31 nt and 22-23 nt processed fragments of the RNY5 gene transcript were identified as active agents.
- Synthetic RNY5 fragments mimicked the cell death-inducing effects of EVs in a dose-dependent manner.
Conclusions:
- Processed RNY5 fragments transferred via EVs represent a novel mechanism for cancer cells.
- This transfer may facilitate cancer cell proliferation and invasion by altering the microenvironment.
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