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MicroRNAs

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MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...

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Related Experiment Video

Updated: Jun 17, 2026

A Reporter Assay to Analyze Intronic microRNA Maturation in Mammalian Cells

A Reporter Assay to Analyze Intronic microRNA Maturation in Mammalian Cells

Published on: June 16, 2022

Interplay between the RBP SYNCRIP and RNA methylation in determining sEV miRNA-cargo and function in cell-to-cell

Luca Quattrocchi¹, Sabrina Garbo¹, Francesco Marocco¹

¹Department of Molecular Medicine, Department of Excellence 2023-2027, Sapienza University of Rome, Rome, Italy.

Cell Death & Disease

|June 15, 2026

Summary

Small extracellular vesicles (sEVs) mediate tumor communication via microRNAs (miRNAs). Researchers found that N6-methyladenosine (m6A) RNA modification and the RNA-binding protein SYNCRIP control miRNA loading into HCC-derived sEVs, impacting tumor progression.

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Last Updated: Jun 17, 2026

A Reporter Assay to Analyze Intronic microRNA Maturation in Mammalian Cells

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Published on: June 16, 2022

mRNA Interactome Capture from Plant Protoplasts

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Published on: July 28, 2017

Isolation of Cognate RNA-protein Complexes from Cells Using Oligonucleotide-directed Elution

Isolation of Cognate RNA-protein Complexes from Cells Using Oligonucleotide-directed Elution

Published on: January 16, 2017

Area of Science:

Molecular Biology
Cancer Research
Cell Biology

Background:

Small extracellular vesicles (sEVs) are key players in tumor microenvironment communication.
MicroRNAs (miRNAs) transferred via sEVs reprogram recipient cells, influencing cancer progression.
The sorting of specific miRNAs into sEVs is regulated by RNA-binding proteins (RBPs) and RNA modifications.

Purpose of the Study:

To investigate the interplay between the RBP SYNCRIP and m6A RNA methylation in controlling miRNA loading into hepatocellular carcinoma (HCC)-derived sEVs.
To elucidate the functional consequences of this interplay on sEV-mediated epithelial-to-mesenchymal transition (EMT) and tumor progression.

Main Methods:

Investigated the binding of SYNCRIP to miRNAs in an m6A-dependent manner.
Utilized gene silencing techniques to assess the impact of METTL3 and SYNCRIP on sEV miRNA cargo.
Evaluated the functional effects of disrupted m6A-SYNCRIP interaction on sEV-induced EMT in non-tumorigenic hepatocytes.

Main Results:

METTL3-dependent m6A modification is essential for SYNCRIP binding to specific miRNAs, facilitating their selective incorporation into sEVs.
Silencing SYNCRIP altered the miRNA cargo of HCC sEVs and impaired their ability to induce EMT.
Depletion of METTL3 had a more pronounced effect than SYNCRIP depletion, highlighting m6A methylation as an upstream regulator.
SYNCRIP acts as an m6A-dependent miRNA reader, integrating epitranscriptomic regulation into miRNA sorting into sEVs.

Conclusions:

A novel regulatory axis involving m6A modification and SYNCRIP governs miRNA selection for export via sEVs.
Disruption of the m6A-SYNCRIP interaction attenuates sEV-driven EMT and pro-tumorigenic signaling.
The m6A-SYNCRIP interplay represents a potential therapeutic target to inhibit sEV-mediated tumor progression and metastasis.