Cross-Talk between Oxidative Stress and m6A RNA Methylation in Cancer

Abstract

Oxidative stress is a state of imbalance between oxidation and antioxidation. Excessive ROS levels are an important factor in tumor development. Damage stimulation and excessive activation of oncogenes cause elevated ROS production in cancer, accompanied by an increase in the antioxidant capacity to retain redox homeostasis in tumor cells at an increased level. Although moderate concentrations of ROS produced in cancer cells contribute to maintaining cell survival and cancer progression, massive ROS accumulation can exert toxicity, leading to cancer cell death. RNA modification is a posttranscriptional control mechanism that regulates gene expression and RNA metabolism, and m⁶A RNA methylation is the most common type of RNA modification in eukaryotes. m⁶A modifications can modulate cellular ROS levels through different mechanisms. It is worth noting that ROS signaling also plays a regulatory role in m⁶A modifications. In this review, we concluded the effects of m⁶A modification and oxidative stress on tumor biological functions. In particular, we discuss the interplay between oxidative stress and m⁶A modifications.