m6A-centered Crosstalk Information
Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
| Crosstalk ID |
M6ACROT05503
|
[1] | |||
m6A modification
hsa-miR-766-5p
hsa-miR-766-5p
METTL3
Methylation
: m6A sites
Direct
Enhancement
Non-coding RNA
miR-766-5p
CDKN1A
lncRNA miRNA circRNA
|
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| m6A Modification: | |||||
|---|---|---|---|---|---|
| m6A Regulator | Methyltransferase-like 3 (METTL3) | WRITER | |||
| m6A Target | hsa-miR-766-5p | ||||
| Epigenetic Regulation that have Cross-talk with This m6A Modification: | |||||
| Epigenetic Regulation Type | Non-coding RNA (ncRNA) | ||||
| Epigenetic Regulator | hsa-miR-766-5p | microRNA | View Details | ||
| Regulated Target | Cyclin-dependent kinase inhibitor 1 (CDKN1A) | View Details | |||
| Crosstalk Relationship | m6A → ncRNA | Enhancement | |||
| Crosstalk Mechanism | m6A regulators directly modulate the functionality of ncRNAs through specific targeting ncRNA | ||||
| Crosstalk Summary | METTL3-mediated m6A modification induced the aberrant expression of NEAT1 in chronic myelocytic leukemia. Overexpression of NEAT1 inhibited cell viability and promoted the apoptosis of chronic myelocytic leukemia cells. hsa-miR-766-5p was upregulated in CML PBMCs and abrogated the effects of NEAT1 on cell viability and apoptosis of the chronic myelocytic leukemia cells. Cyclin-dependent kinase inhibitor 1 (CDKN1A) was proved to be the target gene of miR-766-5p and was downregulated in the CML PBMCs. | ||||
| Responsed Disease | Chronic myeloid leukaemia | ICD-11: 2B33.2 | |||
| Cell Process | Cell viability | ||||
| Cell apoptosis | |||||
In-vitro Model |
K-562 | Chronic myelogenous leukemia | Homo sapiens | CVCL_0004 | |
| KCL-22 | Chronic myelogenous leukemia | Homo sapiens | CVCL_2091 | ||
| MEG-01 | Chronic myelogenous leukemia | Homo sapiens | CVCL_0425 | ||
| BV-173 | Chronic myelogenous leukemia | Homo sapiens | CVCL_0181 | ||
: m6A sites