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
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
References
Ref 1 m(6)A Modification of lncRNA NEAT1 Regulates Chronic Myelocytic Leukemia Progression via miR-766-5p/CDKN1A Axis. Front Oncol. 2021 Jul 20;11:679634. doi: 10.3389/fonc.2021.679634. eCollection 2021.