Advances in research on RNA methylation and cancer radiotherapy resistance

TL;DR

This review explores how RNA methylation affects cancer cells' resistance to radiotherapy and highlights recent findings on potential therapeutic strategies.

Contribution

The paper provides a comprehensive overview of RNA methylation's role in cancer radioresistance and its clinical implications.

Findings

RNA methylation modifications like m6A, m5C, m7G, and m1A influence cancer radioresistance.

Enzymatic systems regulate RNA methylation, impacting gene expression and cancer progression.

Targeting RNA methylation shows potential for improving cancer radiotherapy outcomes.

Abstract

RNA methylation is a type of reversible chemical modification in epitranscriptomics that influences gene expression by dynamically regulating RNA functions. RNA methylation comprises N6-methyladenosine (m6A), 5-methylcytosine (m5C), N7-methylguanosine (m7G), N1-methyladenosine (m1A), and 3-methylcytosine (m3C) modifications. These are dynamically controlled by a tripartite enzymatic system: methyltransferases (“writers”) add methyl groups, demethylases (“erasers”) remove them, and RNA-binding proteins (“readers”) recognize and interpret the modifications to mediate downstream biological effects. Extensive research has shown the importance of RNA methylation in the onset and progression of cancer. RNA methylation contributes to radioresistance in cancer cells through various mechanisms, affecting therapeutic outcomes. To date, the precise functions of RNA methylation in cancer radioresistance remain unclear. This review summarizes recent advances in m6A, m5C, m7G, and m1A methylation in cancer radioresistance regulation and discusses the clinical potential of precision therapeutic strategies targeting these methylation modifications.

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