Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT05521
[1]
m6A modification FOXD2-AS1 FOXD2-AS1 METTL3 Methylation : m6A sites Direct Enhancement Non-coding RNA FOXD2-AS1 CDKN1A  lncRNA       miRNA   circRNA
m6A Modification:
m6A Regulator Methyltransferase-like 3 (METTL3) WRITER
m6A Target FOXD2 adjacent opposite strand RNA 1 (FOXD2-AS1)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type Non-coding RNA (ncRNA)
Epigenetic Regulator FOXD2 adjacent opposite strand RNA 1 (FOXD2-AS1) LncRNA 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/FOXD2 adjacent opposite strand RNA 1 (FOXD2-AS1) accelerates cervical cancer progression via a m6A-dependent modality, which serves as a potential therapeutic target for cervical cancer. FOXD2-AS1 recruited lysine-specific demethylase 1 (LSD1) to the promoter region of Cyclin-dependent kinase inhibitor 1 (CDKN1A) to silence its transcription abundance.
Responsed Disease Cervical cancer ICD-11: 2C77
Cell Process Cell migration
Cell proliferation
In-vitro Model
Ca Ski Cervical squamous cell carcinoma Homo sapiens CVCL_1100
HT-3 Cervical carcinoma Homo sapiens CVCL_1293
SiHa Cervical squamous cell carcinoma Homo sapiens CVCL_0032
C-33 A Cervical squamous cell carcinoma Homo sapiens CVCL_1094
HaCaT Normal Homo sapiens CVCL_0038
In-vivo Model A total 5 × 106 stably transfected SiHa cells were subcutaneously injected into the flank of nude mice.
References
Ref 1 m(6)A methyltransferase METTL3-mediated lncRNA FOXD2-AS1 promotes the tumorigenesis of cervical cancer. Mol Ther Oncolytics. 2021 Jul 21;22:574-581. doi: 10.1016/j.omto.2021.07.004. eCollection 2021 Sep 24.