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. 2023 Feb 26;9(3):e14001. doi: 10.1016/j.heliyon.2023.e14001

Table 2.

m6A modulations in cancer therapeutic resistance.

Cancers m6A-enymases Drug resistance Mechanisms References
NSCLC METTL3 Increase resistance to DDP MALAT1-miR-1914-3p-YAP axis via recruiting YTHDF1/3 and eIF3b [93]
Lung cancer m6A modulation Increase resistance to afatinib m6A-modified genes increase [94]
Melanoma FTO Increase resistance to IFNγ and anti-PD-1 treatment Inhibit m6A methylation of protumorigenic melanoma cell-intrinsic genes including PD-1 (PDCD1), CXCR4, and SOX10 [99]
Leukemia FTO Increase resistance to TKIs Regulate mRNA stability of proliferation/survival transcripts bearing m6A and protein synthesis [100]
CSCC FTO Increase chemo-radiotherapy resistance Decrease m6A methylation of β-catenin and then increase ERCC1 activity [101]
PDAC ALKBH5 Decrease resistance to gemcitabine Change its target genes via Global m6A profile [102]
BRCA-mutated EOC cells FTO and ALKBH5 m6A modification of FZD10 mRNA increase resistance to PARPi Wnt/β-catenin pathway induces m6A modification of FZD10 mRNA via downregulation of FTO and ALKBH5 [19]
Colon cancer m6A methylation CBX8 increases chemoresistance m6A methylation promotes CBX8 mRNA stability to increase CBX8 [103]
OSCC ALKBH5 DDX3 increase resistance to cisplatin DDX3 modulates ALKBH5 to reduce m6A methylation in FOXM1 and NANOG nascent transcript and increases CSC population [104]

NSCLC: non-small cell lung cancer; CSCC: Cervical squamous cell carcinoma; PDAC: pancreatic ductal adenocarcinoma; EOC: epithelial ovarian cancers; OSCC: Oral squamous cell carcinoma.