Quantifying the mRNA epitranscriptome reveals epitranscriptome signatures and roles in cancer

Abstract Post-transcriptional modifications on mRNA are crucial for mRNA fate and function. The current lack of a comprehensive method for high-coverage and sensitive quantitative analysis of mRNA modifications significantly limits the discovery of new mRNA modifications and understanding mRNA modif...

Full description

Saved in:
Bibliographic Details
Main Authors: Ying Feng, Xiaoli He, Mingxin Guo, Ying Tang, Guantong Qi, Qian Huang, Wenran Ma, Hong Chen, Yifan Qin, Ruiqi Li, Jin Wang, Yu Liu
Format: Article
Language:English
Published: Springer 2025-07-01
Series:Cellular and Molecular Life Sciences
Subjects:
Online Access:https://doi.org/10.1007/s00018-025-05805-7
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Abstract Post-transcriptional modifications on mRNA are crucial for mRNA fate and function. The current lack of a comprehensive method for high-coverage and sensitive quantitative analysis of mRNA modifications significantly limits the discovery of new mRNA modifications and understanding mRNA modifications’ occurrence, dynamics and function. Here, a highly sensitive, high-throughput and robust LC-MS/MS-based technique, mRQuant, was developed to simultaneously detect and quantify 84 modified ribonucleosides in cellular mRNA. Using mRQuant, we quantified 32–34 modified ribonucleosides across several human cancer and non-cancer cell lines and uncovered cancer- and cancer type-specific signatures. Analyses of cisplatin- and paclitaxel-treated HeLa cells and drug-resistant variants revealed several drug resistance-associated modifications. Among them, m1A exhibited significant differences across multiple cell types and between cancerous and non-cancerous cells. Knocking down mRNA m1A writer or eraser protein resulted in altered cell viability, cell cycle and apoptosis in HeLa cells, suggesting a role of mRNA m1A in cancer. Transcriptomic and proteomic analyses further revealed the molecular mechanisms underlying the phenotypic variation.
ISSN:1420-9071