Table 3.
m6A enzyme | Change of m6A modification | ROS levels | Cancer type | Mechanism | Biofunction in cancer | References |
---|---|---|---|---|---|---|
METTL3; ALKBH5 | m6A level↑ | ↑ | Breast cancer | METTL3 enhances AK4 expression, increase the level of ROS in breast cancer cells and activate p38 Kinase | Promoting the resistance of breast cancer to Tamoxifen | [226] |
METTL3 | Unknown | ↑ | Colorectal cancer | METTL3 facilitates the processing of miR-483, miR-676, and miR-877 which regulating the expression of mitochondrial related ETC genes | Promoting cancer growth and progression | [225] |
METTL3; METTL14 | Unknown | ↓ | Colon carcinoma | METTL3/METTL14 catalyzes the m6A methylation of p21 and enhances p21 expression leading to elevated expression of Nrf2 | Inducing cell senescence | [208, 229] |
FTO | Unknown | ↑ | Clear cell renal cell carcinoma | FTO increases stability and translation of PGC-1α mRNA thereby resulting in oxidative stress | Inducing ROS production and suppressing tumor growth | [227] |
YTHDF1 | YTHDF1↓ | ↓ | Nonsmall cell lung cancer | Knockdown of YTHDF1 reduces the translation of keap, upregulates Nrf2 and its downstream antioxidant in response of cisplatin-induced ROS | Adapting to oxidative stress; Inducing cisplatin resistance in nonsmall cell lung cancer | [215] |
METTL3; YTHDF2 | METTL3↑ SUMOylation of YTHDF2 |
↑ | Lung adenocarcinoma | YTHDF2 can be SUMOylated at K571 in hypoxia or oxidative stress condition | Promoting mRNA degradation and cancer progression | [21] |
YTHDC2 | Unknown | ↑ | Lung adenocarcinoma | YTHDC2 regulates SLC7A11 mRNA decay, which leads to the inhibition system XC(-) function, thus impairing the antioxidant function | Inhibiting tumorigenesis | [233] |