Language

English

Publication Date

6-6-2024

Journal

Molecular Cell

DOI

10.1016/j.molcel.2024.05.004

PMID

38815579

PMCID

PMC11204102

PubMedCentral® Posted Date

6-6-2025

PubMedCentral® Full Text Version

Author MSS

Abstract

RNA splicing is pivotal in post-transcriptional gene regulation, yet the exponential expansion of intron length in humans poses a challenge for accurate splicing. Here, we identify hnRNPM as an essential RNA-binding protein that suppresses cryptic splicing through binding to deep introns, maintaining human transcriptome integrity. Long interspersed nuclear elements (LINEs) in introns harbor numerous pseudo splice sites. hnRNPM preferentially binds at intronic LINEs to repress pseudo splice site usage for cryptic splicing. Remarkably, cryptic exons can generate long dsRNAs through base-pairing of inverted ALU transposable elements interspersed among LINEs and consequently trigger an interferon response, a well-known antiviral defense mechanism. Significantly, hnRNPM-deficient tumors show upregulated interferon-associated pathways and elevated immune cell infiltration. These findings unveil hnRNPM as a guardian of transcriptome integrity by repressing cryptic splicing and suggest that targeting hnRNPM in tumors may be used to trigger an inflammatory immune response, thereby boosting cancer surveillance.

Keywords

Humans, Heterogeneous-Nuclear Ribonucleoprotein Group M, RNA, Double-Stranded, Introns, RNA Splicing, Long Interspersed Nucleotide Elements, Interferons, Animals, HEK293 Cells, Mice, Transcriptome, Exons, RNA Splice Sites, Alu Elements, Cryptic splicing, hnRNPM, RNA binding protein, LINE, ALU, double-stranded RNA, interferon response, cancer

Published Open-Access

yes

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