Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT05520
[1]
m6A modification HOXC13-AS HOXC13-AS FTO Demethylation : m6A sites Direct Enhancement Non-coding RNA HOXC13-AS Regulated Target  lncRNA       miRNA   circRNA
m6A Modification:
m6A Regulator Fat mass and obesity-associated protein (FTO) ERASER
m6A Target HOXC13 antisense RNA (HOXC13-AS)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type Non-coding RNA (ncRNA)
Epigenetic Regulator HOXC13 antisense RNA (HOXC13-AS) LncRNA View Details
Crosstalk Relationship m6A  →  ncRNA Enhancement
Crosstalk Mechanism m6A regulators directly modulate the functionality of ncRNAs through specific targeting ncRNA
Crosstalk Summary FTO-stabilized HOXC13 antisense RNA (HOXC13-AS) epigenetically up-regulated FZD6 and activated Wnt/beta-catenin signaling to drive cervical cancer proliferation, invasion, and EMT, suggesting HOXC13-AS as a potential target for cervical cancer treatment.
Responsed Disease Cervical cancer ICD-11: 2C77
Pathway Response Wnt signaling pathway hsa04310
Cell Process Cell proliferation
Cell invasion
Epithelial-mesenchymal transition
In-vitro Model
C-33 A Cervical squamous cell carcinoma Homo sapiens CVCL_1094
C-4-I Cervical squamous cell carcinoma Homo sapiens CVCL_2253
HeLa Endocervical adenocarcinoma Homo sapiens CVCL_0030
SiHa Cervical squamous cell carcinoma Homo sapiens CVCL_0032
References
Ref 1 FTO-stabilized lncRNA HOXC13-AS epigenetically upregulated FZD6 and activated Wnt/Beta-catenin signaling to drive cervical cancer proliferation, invasion, and EMT. J BUON. 2021 Jul-Aug;26(4):1279-1291.