Table 1.
The roles of m6A modification on coding RNAs in CRC
| Regulator | Role | Target mRNA | Function | Mechanism | Ref |
|---|---|---|---|---|---|
| Writer | |||||
| METTL3 | Oncogene | SOX2 | promoted CRC metastasis | maintained SOX2 expression through an m6A-IGF2BP2-dependent way. | [31] |
| MYC | promoted CRC proliferation and tumorigenesis | enhance MYC expression in an m6A IGF2BP1-dependent manner. | [38] | ||
| YPEL5 | promoted CRC tumorigenesis | repressed YPEL5 by targeting the m6A site in the coding sequence region of the YPEL5 transcript. | [39] | ||
| Sec62 | promoted stemness and chemoresistance of CRC | enhanced Sec62 mRNA stability by controlling its m6A modification. | [40] | ||
| HSF1 | promoted CRC development | promoted HSF1 mRNA translation. | [46] | ||
| HK2 and SLC2A1/GLUT1 |
promoted CRC tumorigenesis | stabilized HK2 and SLC2A1/GLUT1 expression. | [41] | ||
| GLUT1 | promoted CRC tumorigenesis | promoted GLUT1 translation and glucose metabolism. | [47] | ||
| SOCS2 | promoted CRC tumorigenesis | regulated SOCS2 RNA stability with m6A modification. | [42] | ||
| CCNE1 | promoted CRC proliferation | stabilized CCNE1 mRNA. | [43] | ||
| CBX8 | associated with stemness properties in CRC | induced aberrant overexpression of CBX8. | [44] | ||
| HMGA1 | promoted CRC metastasis | regulated HMGA1 expression through an m6A-dependent mechanism. | [45] | ||
| Anti-oncogene | - | suppressed CRC proliferation migration and invasion | modulated the p38/ERK pathways through an m6A-dependent way. | [48] | |
| METTL14 | Anti-oncogene | SOX4 | suppressed CRC progress | inhibited SOX4-mediated EMT process and PI3K/AKT signalling pathway. | [32] |
| KLF4 | suppressed CRC metastasis | regulated the expression of tumour suppressor KLF4 through changing m6A modification level. | [49] | ||
| Eraser | |||||
| FTO | Oncogene | MZF1 | promoted CRC proliferation | activated MZF1/c-Myc axis to promote CRC cell proliferation. | [52] |
| MYC | promoted CRC progress | activated MYC by reducing the m6A modification of MYC. | [53] | ||
| Anti-oncogene | MTA1 | suppressed CRC metastasis | Regulated the MTA1 expression in an m6A-dependent manner | [55] | |
| Reader | |||||
| YTHDF1 | Oncogene | FZD9/WNT6 | promoted CRC tumorigenesis | recognized and promoted the translation of m6A-modified FZD9 and Wnt6 mRNA | [58] |
| YTHDF2 | Anti-oncogene | SOX4 | inhibited CRC progress | modulated m6A-dependent SOX4 mRNA degradation. | [32] |
| Oncogene | YPEL5 | promoted CRC progress | suppressed the expression of YPEL5 | [34] | |
| YTHDC2 | Oncogene | HIF-1α | promoted CRC proliferation | stabilize HIF-1α mRNA | [62] |
| IGF2BP1 | Oncogene | MYC | promoted CRC progress | recognized the m6A modification sites on MYC to enhance its mRNA stability and translation. | [38,79] |
| Sec62 | promoted stemness and chemoresistance of CRC | bound to the m6A-modified Sec62 mRNA to maintain the Sec62 mRNA stability. | [40] | ||
| IGF2BP2 | Oncogene | SOX2 | promoted CRC progress | prevented SOX2 mRNA degradation in a m6A-dependent manner. | [31] |
| HMGA1 | promoted CRC progress | regulated HMGA1 mRNA stability in a m6A-dependent manner. | [45] | ||
| HMGA2 | promoted CRC progress | regulated HMGA2 mRNA stability | [63] | ||
| MYC | promoted CRC progress | recognized the m6A modification sites on MYC to enhance its mRNA stability | [82] | ||
| IGF2BP2/3 | Oncogene | HK2 and SLC2A1/GLUT1 | promoted CRC tumorigenesis | stabilized HK2 and SLC2A1/GLUT1 expression. | [41] |