m6A-centered Crosstalk Information
Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
| Crosstalk ID |
M6ACROT05364
|
[1] | |||
Non-coding RNA
LINC00470
METTL3
lncRNA miRNA circRNA
Direct
Enhancement
m6A modification
PTEN
PTEN
METTL3
Methylation
: m6A sites
|
|||||
| m6A Modification: | |||||
|---|---|---|---|---|---|
| m6A Regulator | Methyltransferase-like 3 (METTL3) | WRITER | |||
| m6A Target | Mutated in multiple advanced cancers 1 (PTEN) | ||||
| Epigenetic Regulation that have Cross-talk with This m6A Modification: | |||||
| Epigenetic Regulation Type | Non-coding RNA (ncRNA) | ||||
| Epigenetic Regulator | Long intergenic non-protein coding RNA 470 (LINC00470) | LncRNA | View Details | ||
| Regulated Target | Methyltransferase-like protein 3 (METTL3) | View Details | |||
| Crosstalk Relationship | ncRNA → m6A | Enhancement | |||
| Crosstalk Mechanism | ncRNAs directly impacts m6A modification through recruiting m6A regulator | ||||
| Crosstalk Summary | Our results demonstrated the molecular mechanism underlying the effect of LINC00470 on CML by reducing the Mutated in multiple advanced cancers 1 (PTEN) stability via RNA methyltransferase METTL3, thus leading to the inhibition of cell autophagy while promoting chemoresistance in CML. | ||||
| Responsed Disease | Chronic myeloid leukaemia | ICD-11: 2B33.2 | |||
| Pathway Response | Autophagy | hsa04140 | |||
| Cell Process | RNA stability | ||||
| Cell autophagy | |||||
: m6A sites