Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT00531
[1], [2], [3]
m6A modification H19 H19 METTL3 Methylation : m6A sites Indirect Enhancement RNA modification MIR19A MIR19A ADAR Methylation : modification sites
m6A Modification:
m6A Regulator Methyltransferase-like 3 (METTL3) WRITER
m6A Target H19 imprinted maternally expressed transcript (H19)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type RNA modification (RNAMod)  >> Adenosine-to-Inosine editing (A-to-I)
Epigenetic Regulator Interferon-inducible protein 4 (ADAR1) WRITER View Details
Regulated Target MicroRNA 19a (MIR19A) View Details
Crosstalk Relationship m6A  →  A-to-I Enhancement
Crosstalk Mechanism m6A modification indirectly impacts RNA modification through downstream signaling pathways
Crosstalk Summary METTL3 interacts with H19 imprinted maternally expressed transcript (H19), increasing its m6A level and promoting its physical interaction with MicroRNA 19a (MIR19A), which was regulated by ADAR1-mediated A-to-I modification.
In-vitro Model
MGG8 Glioblastoma Homo sapiens CVCL_D1H4
HN4 Clear cell renal cell carcinoma Homo sapiens CVCL_IS30
CAL-27 Tongue squamous cell carcinoma Homo sapiens CVCL_1107
References
Ref 1 N?-Methyladenosine Landscape of Glioma Stem-Like Cells: METTL3 Is Essential for the Expression of Actively Transcribed Genes and Sustenance of the Oncogenic Signaling. Genes (Basel). 2019 Feb 13;10(2):141. doi: 10.3390/genes10020141.
Ref 2 ADAR1 promotes the epithelial-to-mesenchymal transition and stem-like cell phenotype of oral cancer by facilitating oncogenic microRNA maturation. J Exp Clin Cancer Res. 2019 Jul 17;38(1):315. doi: 10.1186/s13046-019-1300-2.
Ref 3 Blocking lncRNA H19-miR-19a-Id2 axis attenuates hypoxia/ischemia induced neuronal injury. Aging (Albany NY). 2019 Jun 5;11(11):3585-3600. doi: 10.18632/aging.101999.