From: Novel insights on m6A RNA methylation in tumorigenesis: a double-edged sword
Tumour Type | Gene involved | Gene function | Description | reference |
---|---|---|---|---|
Acute myeloid leukaemia | ASB2 RARA | Anti-oncogene | Elevated FTO leads to low levels of m6A on ASB2 and RARA at UTRs, which reduces the mRNA and protein levels of these two genes | [47] |
MYB MYC | Oncogene | METTL14 enhances m6A modification of MYB and MYC, which in turn leads to overexpression of MYB and MYC | [48] | |
BCL2 PTEN | Oncogene | Increased METTL3 in AML enhances m6A modification of BCL2 and PTEN, which leads to overexpression of BCL2 and PTEN | [50] | |
SP1 | Oncogene | METTL3 binds to the promoter region of sp1 and enhances m6A modification and gene expression | [51] | |
Hepatocellular carcinoma | SOCS2 | Anti-oncogene | High expression of METTL3 in human HCC leads to high m6A levels on SOCS2, causing the rapid degradation of SOCS2 | [60] |
microRNA126 | Anti-oncogene | Decreased METTL14 reduces m6A modification levels and the expression of microRNA126 | [61] | |
Glioblastoma stem cells | ADAM19 | Oncogene | Low levels of METTL3 and METTL14 decrease m6A modification of ADAM19, which enhances the expression of ADAM19 | [69] |
FOXM1 | Oncogene | High levels of ALKBH5 decrease m6A modification levels of FOXM1 and enhance the expression of FOXM1, which ultimately causes glioblastoma | [70] | |
Breast cancer | KLF4 NANOG | Oncogene | ZNF217 interacts with METTL3 and inhibits the m6A methylation of KLF4 and NANOG, which ultimately leads to high expression of KLF4 and NANOG | [74] |
HBXIP | Oncogene | High levels of METTL3 enhance m6A modification of HBXIP, which accelerates HBXIP expression | [75] | |
MAGI3 | Anti-oncogene | High levels of m6A modification in the large internal exon of MAGI3 promote the occurrence of breast cancer | [31] | |
Cervical cancer | β-catenin | Anti-oncogene | Upregulated FTO represses m6A modification of β-catenin and induces chemoradiotherapy resistance | [79] |