Table 1.

A summary of mRNA modification and cancer stem cells

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	[49, 50]
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]