# m6A RNA modification and myeloid-derived suppressor cells: mechanistic insights and clinical prospects

## TL;DR

This paper reviews how m6A RNA modification influences myeloid-derived suppressor cells in cancer, highlighting its role in tumor progression and potential for immunotherapy.

## Contribution

The paper provides a comprehensive review of the molecular mechanisms linking m6A modification to MDSC function in cancer.

## Key findings

- m6A modification regulates MDSC differentiation and immunosuppressive activity in the tumor microenvironment.
- Altered m6A levels contribute to tumor progression by promoting immune evasion and therapy resistance.
- Understanding m6A-MDSC interactions may lead to new strategies for cancer immunotherapy.

## Abstract

N6-methyladenosine (m6A) is the most abundant post-transcriptional modification in eukaryotic mRNA, extensively involved in RNA splicing, export, stability, and translation. In recent years, accumulating evidence has demonstrated that m6A modification plays a critical role in regulating the differentiation and function of immune cells. Among these, myeloid-derived suppressor cells (MDSCs), as a key immunosuppressive population within the tumor microenvironment (TME), accelerate tumor progression by inhibiting T cell activity and promoting immune evasion and therapy resistance. Emerging studies indicate that m6A modification modulates the development, accumulation, and immunosuppressive function of MDSCs, thereby contributing to tumor initiation and progression. This review provides a narrative overview of the current evidence regarding the crosstalk between m6A modification and MDSCs, with a focus on the underlying molecular mechanisms and their potential implications for cancer immunotherapy. Furthermore, we discuss future research directions and the challenges associated with clinical translation.