m6A-centered Crosstalk Information
Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
| Crosstalk ID |
M6ACROT00070
|
[1], [2] | |||
: modification sites
Direct
Enhancement
m6A modification
SOCS2
SOCS2
METTL3
Methylation
: m6A sites
|
|||||
| m6A Modification: | |||||
|---|---|---|---|---|---|
| m6A Regulator | Methyltransferase-like 3 (METTL3) | WRITER | |||
| m6A Target | Suppressor of cytokine signaling 2 (SOCS2) | ||||
| Epigenetic Regulation that have Cross-talk with This m6A Modification: | |||||
| Epigenetic Regulation Type | RNA modification (RNAMod) >> 5-methylcytidine (m5C) | ||||
| Epigenetic Regulator | tRNA (cytosine(72)-C(5))-methyltransferase NSUN6 (NSUN6) | WRITER | View Details | ||
| Regulated Target | Methyltransferase-like protein 3 (METTL3) | View Details | |||
| Crosstalk Relationship | m5C → m6A | Enhancement | |||
| Crosstalk Mechanism | RNA modification directly impacts m6A modification through modulating the expression level of m6A regulator | ||||
| Crosstalk Summary | NSUN6 upregulates the expression of oncogenic METTL3 and catalyzes its m5C modification in COAD cells. Overexpression of METTL3 significantly relieved the cell cycle inhibition of COAD caused by NSUN6 deficiency.An increased level of METTL3 may maintain the tumorigenicity of colon cancer cells by suppressing Suppressor of cytokine signaling 2 (SOCS2). | ||||
| Responsed Disease | Colon cancer | ICD-11: 2B90 | |||
| Cell Process | Colon adenocarcinoma | ||||
In-vitro Model |
HCT 116 | Colon carcinoma | Homo sapiens | CVCL_0291 | |
| HCT 8 | Colon adenocarcinoma | Homo sapiens | CVCL_2478 | ||
| SW480 | Colon adenocarcinoma | Homo sapiens | CVCL_0546 | ||
| NCM460 | Normal | Homo sapiens | CVCL_0460 | ||
References
: modification sites
: m6A sites