Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT05151
[1], [2]
Non-coding RNA miR-103-3p METTL14  lncRNA       miRNA   circRNA Direct Inhibition m6A modification NFATC1 NFATC1 METTL14 Methylation : m6A sites
m6A Modification:
m6A Regulator Methyltransferase-like 14 (METTL14) WRITER
m6A Target Nuclear factor of activated T-cells, cytoplasmic 1 (NFATC1)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type Non-coding RNA (ncRNA)
Epigenetic Regulator hsa-miR-103-3p microRNA View Details
Regulated Target Methyltransferase-like protein 14 (METTL14) View Details
Crosstalk Relationship ncRNA  →  m6A Inhibition
Crosstalk Mechanism ncRNAs directly impacts m6A modification through modulating the expression level of m6A regulator
Crosstalk Summary hsa-miR-103-3p targets the m6 A methyltransferase METTL14 to inhibit osteoblastic bone formation.METTL14 released by exosomes can increase the m6A methylation level of Nuclear factor of activated T-cells, cytoplasmic 1 (NFATC1) to inhibit osteoclasts, help postmenopausal osteoporosis patients preserve bone mass, and avoid triggering osteonecrosis of the jaw, thus becoming a new bioactive molecule for the treatment of osteoporosis.
Responsed Disease Osteoporosis ICD-11: FB83.1
In-vitro Model
RAW 264.7 Mouse leukemia Mus musculus CVCL_0493
MC3T3-E1 Normal Mus musculus CVCL_0409
References
Ref 1 MiR-103-3p targets the m(6) A methyltransferase METTL14 to inhibit osteoblastic bone formation. Aging Cell. 2021 Feb;20(2):e13298. doi: 10.1111/acel.13298. Epub 2021 Jan 13.
Ref 2 Exosome-targeted delivery of METTL14 regulates NFATc1 m6A methylation levels to correct osteoclast-induced bone resorption. Cell Death Dis. 2023 Nov 13;14(11):738. doi: 10.1038/s41419-023-06263-4.