Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT05152
[1], [2]
Non-coding RNA miR-103-3p METTL14  lncRNA       miRNA   circRNA Direct Inhibition m6A modification SLC2A3 SLC2A3 METTL14 Methylation : m6A sites
m6A Modification:
m6A Regulator Methyltransferase-like 14 (METTL14) WRITER
m6A Target Solute carrier family 2, facilitated glucose transporter member 3 (SLC2A3)
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 promotes Solute carrier family 2, facilitated glucose transporter member 3 (SLC2A3) expression via YTHDF1, leading to the modulation of various parameters in the H2O2-induced model. Similar positive effects of METTL14 on osteogenesis were observed in an ovariectomized mouse osteoporosis model. DISCUSSION METTL14 could serve as a potential therapeutic approach for enhancing osteoporosis treatment.
Responsed Disease Osteoporosis ICD-11: FB83.1
In-vitro Model
MC3T3-E1 Normal Mus musculus CVCL_0409
In-vivo Model Female C57BL/6 mice, aged eight weeks, were selected for the study. The mice were divided into three groups with six mice per group. After intramuscular anesthesia (xylazine 10 mg/kg, ketamine 100 mg/kg), two groups underwent bilateral ovariectomy (OVX), while the remaining group had a sham operation. Ovariectomized mice were administered weekly intratibial injections of Mettl14 overexpression adenovirus containing at a concentration of 109 plaque-forming unit per injection, for a duration of 8 weeks. The mice were humanely euthanized one week after the final injection, and their tibia were gathered for further analysis. This study was approved by the ethics committee of Tongji University (NO: TJBH00823101). All the experimental methods were carried out in accordance with the approved guidelines. All experimental procedures involving mice were carried out in strict accordance with the recommendations in the ARRIVE guidelines (Animal Research: Reporting of In Vivo Experiments).
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 METTL14 Mediates Glut3 m6A methylation to improve osteogenesis under oxidative stress condition. Redox Rep. 2025 Dec;30(1):2435241. doi: 10.1080/13510002.2024.2435241. Epub 2024 Dec 31.