From: mRNA modification orchestrates cancer stem cell fate decisions
Cancer cell types | RNA modification | Expression profiles in CSC | Molecular mechanisms | References |
---|---|---|---|---|
Leukemia | A-to-I | Increased | A-to-I editing induced alternative splicing of GSK3β, resulting in enhanced β-catenin expression | |
Multiple myeloma | A-to-I | Increased | A-to-I editing occurred in the exon of GLI1 mRNA, leading to a novel GLI1 protein with a point mutation | [51] |
Leukemia | A-to-I | Increased | A-to-I editing occurred in the 3’UTR of MDM2 mRNA and miR-155 would no longer bind to the edited 3’UTR region | [52] |
Leukemia | A-to-I | Increased | A-to-I editing in let-7 precursor impaired let-7 biogenesis | [36] |
Skin cancer | m5C | Decreased | NSUN2-deletion impaired protein synthesis | [53] |
Breast cancer | m6A | Decreased | ALKBH5 reduced m6A level of NANOG, which stabilized NANOG mRNA | [33] |
Glioblastoma | m6A | Decreased | Knockdown of METTL3 or METTL14 in CSCs increased the expression of ADAM19 and EPHA3 | [34] |
Glioblastoma | m6A | Decreased | ALKBH5 demethylated FOXM1 mRNA transcripts and stabilized FOXM1 | [35] |
Glioblastoma | m6A | Increased | SOX2 was a target for METTL3 and methylated SOX2 mRNA displayed prolonged stability | [54] |
Leukemia | m6A | Decreased | Treatment with FTO inhibitor R-2HG induced the degradation of MYC/CEBPA mRNAs | [55] |
Leukemia | m6A | Increased | METTL14 catalyzed the m6A modification in oncogenic factors MYC and MYB, increasing their mRNA stability | [56] |