m6A Target Gene Information

General Information of the m6A Target Gene (ID: M6ATAR00025)
Target Name hsa-miR-126-5p
Synonyms
hsa_miR_126_5p
    Click to Show/Hide
Gene Name hsa-miR-126-5p
miRBase ID
MIMAT0000444
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
hsa-miR-126-5p can be regulated by the following regulator(s), and cause disease/drug response(s). You can browse detail information of regulator(s) or disease/drug response(s).
Browse Regulator
Browse Disease
Methyltransferase-like 3 (METTL3) [WRITER]
 Regulator Info 
In total 2 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary METTL3 promoted the maturation of hsa-miR-126-5p via the m6A modification of pri-miR-126-5p. Finally, in vitro and in vivo experiments substantiated that silencing of METTL3 impeded the progression and tumorigenesis of ovarian cancer by impairing the miR-126-5p-targeted inhibition of PTEN and thus blocking the PI3K/Akt/mTOR pathway.
Target Regulation Up regulation
Responsed Disease Ovarian cancer ICD-11: 2C73
 Disease Info 
Cell Process Cell proliferation
Cell migration
Cell invasion
Experiment 2 Reporting the m6A Methylation Regulator of This Target Gene [2]
Response Summary Interleukin 1-beta (IL-1-beta) is an important inducer of cartilage degeneration that can induce an inflammatory cascade reaction in chondrocytes and inhibit the normal biological function of cells. METTL3 could regulate hsa-miR-126-5p maturation, we first confirmed that METTL3 can bind the key protein underlying pri-miRNA processing, DGCR8. Additionally, when METTL3 expression was inhibited, the miR-126-5p maturation process was blocked.
Target Regulation Up regulation
Responsed Disease Chondropathies ICD-11: FB82
 Disease Info 
Cell Process RNA mature
In-vitro Model Cartilage cells (From the cartilage tissue samples from patients)
Ovarian cancer [ICD-11: 2C73]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary METTL3 promoted the maturation of hsa-miR-126-5p via the m6A modification of pri-miR-126-5p. Finally, in vitro and in vivo experiments substantiated that silencing of METTL3 impeded the progression and tumorigenesis of ovarian cancer by impairing the miR-126-5p-targeted inhibition of PTEN and thus blocking the PI3K/Akt/mTOR pathway.
Responsed Disease Ovarian cancer [ICD-11: 2C73]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
 Regulator Info 
Target Regulation Up regulation
Cell Process Cell proliferation
Cell migration
Cell invasion
Chondropathies [ICD-11: FB82]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [2]
Response Summary Interleukin 1-beta (IL-1-beta) is an important inducer of cartilage degeneration that can induce an inflammatory cascade reaction in chondrocytes and inhibit the normal biological function of cells. METTL3 could regulate hsa-miR-126-5p maturation, we first confirmed that METTL3 can bind the key protein underlying pri-miRNA processing, DGCR8. Additionally, when METTL3 expression was inhibited, the miR-126-5p maturation process was blocked.
Responsed Disease Chondropathies [ICD-11: FB82]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
 Regulator Info 
Target Regulation Up regulation
Cell Process RNA mature
In-vitro Model Cartilage cells (From the cartilage tissue samples from patients)
References
Ref 1 METTL3-mediated maturation of miR-126-5p promotes ovarian cancer progression via PTEN-mediated PI3K/Akt/mTOR pathway. Cancer Gene Ther. 2021 Apr;28(3-4):335-349. doi: 10.1038/s41417-020-00222-3. Epub 2020 Sep 16.
Ref 2 METTL3 promotes IL-1Beta-induced degeneration of endplate chondrocytes by driving m6A-dependent maturation of miR-126-5p. J Cell Mol Med. 2020 Dec;24(23):14013-14025. doi: 10.1111/jcmm.16012. Epub 2020 Oct 23.