Molecular mechanisms of m6A modifications regulating tumor radioresistance

Abstract

Radiotherapy is one of the most effective treatments for malignant tumors. Radioresistance is a major factor that contributes to radiotherapy failure and poor prognosis. Recent studies have elucidated the pivotal role of aberrant N6-methyladenosine (m6A) modification, the predominant internal mRNA modification in eukaryotic cells, influences cancer progression by disrupting gene expression and other critical cellular processes. Furthermore, aberrant m6A methylation provides a substrate for tumor therapy; however, whether it regulates tumor radioresistance remains unclear. Methylated transferase (writer), demethylated transferase (eraser), and methylated recognition protein (reader) are the three essential proteins that regulate m6A modification via different mechanisms in different tumors. This review summarizes the latest research advances in m6A methylation and aims to provide novel perspectives on the advancement of regimens to overcome radioresistance and tumor invasion.