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

Table 4

ROS regulate m⁶A modification.

Oxidative stress activators	Cell type	Change of m^6A components	Biofunction	References
Low dose of NaAsO2	Human keratinous HaCaT cells	METTL3↑; METTL14↑; WTAP↑; FTO↓	Moderate level of ROS-facilitating cell survival via elevated m^6A levels in HaCaT cells	[208]
High dose of NaAsO2	Human keratinous HaCaT cells	METTL3↓; METTL14↓;WTAP↓;FTO↑	High level of ROS inducing cell death by decreased m^6A levels in HaCaT cells	[208]
Hypoxia	Breast cancer stem cells	ALKBH5↑	Decreasing NANOG mRNA methylation, enhancing the expression of NANOG transcripts, and inducing breast cancer stem cell phenotype	[212]
H2O2	Hematopoietic stem/progenitor cells	ALKBH5 m^6A demethylase activity↓	Participating in DNA damage repair and protecting genomic integrity of cells	[213]
Bmal1 deletion	Hepatic cells	METTL3↑; YTHDF2↑	Increasing PPaRα m^6A abundance, decreasing its expression, and promoting lipid accumulation	[214]
Hypoxia	NSCLC cells	YTHDF1↑	Playing a role in hypoxia adaptation of NSCLC through Keap1-Nrf2-AKR1C1 axis	[215]
Hypoxia	Lung adenocarcinoma cells	YTHDF2 SUMOylation at the Lys571 site	Promoting degradation of transcriptome-wide mRNAs and cancer progression	[21]