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.
Highlights
Reactive oxygen species (ROS) are byproducts of the respiratory chain, which act as important signal transduction molecules in cells [1]
Treatment with H2O2 and N-acetylcysteine (NAC, a kind of ROS scavenger) was shown to alter intracellular ROS levels, and the results showed that the activity of Nuclear factor-κB (NF-κB) increased after exposure to H2O2, while the opposite result was obtained after NAC treatment [122]
The results showed that FB1 induced intracellular ROS accumulation, and the increase in the m6A level was accompanied by increases in both m6A writers, including METLL3 and METLL14, and readers, including YTHDF1, YTHDF2, YTHDF3, and YTHDC2, and decreases in Fat mass and obesity-associated protein (FTO) and alkB homolog 5 (ALKBH5)
Summary
Reactive oxygen species (ROS) are byproducts of the respiratory chain, which act as important signal transduction molecules in cells [1]. The production of ROS is regulated by a variety of intracellular and extracellular stimuli These oxygen-based molecules contain unpaired electrons, and their instability can lead to the irreversible inactivation of intracellular targets such as proteins, nucleic acids, and lipids [2]. Oxidative stress is defined as a relative excess of ROS, which is closely associated with aging-related diseases, such as neurodegenerative disorders [4], cardiovascular diseases [5, 6], and normal senescence [7, 8], and with many other diseases, including cancer. Many oncogenes can affect ROS production in a direct or indirect manner; cancer cells usually show elevated levels of ROS. To adapt to the relatively high levels of ROS and maintain survival and proliferative activity, the antioxidation capability of cancer cells is increased to neutralize the cytotoxicity caused by excessive ROS [9]. We describe the way in which oxidative stress and m6A modification influence biological functions in cancer and discuss the cross-talk between them in this review
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