Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT05541
[1]
m6A modification KCNQ1OT1 KCNQ1OT1 YTHDF2 : m6A sites Direct Enhancement Non-coding RNA KCNQ1OT1 HOXA9  lncRNA       miRNA   circRNA
m6A Modification:
m6A Regulator YTH domain-containing family protein 2 (YTHDF2) READER
m6A Target KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type Non-coding RNA (ncRNA)
Epigenetic Regulator KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) LncRNA View Details
Regulated Target Homeobox A9 (HOXA9) View Details
Crosstalk Relationship m6A  →  ncRNA Enhancement
Crosstalk Mechanism m6A regulators directly modulate the functionality of ncRNAs through specific targeting ncRNA
Crosstalk Summary ALKBH5 mediates KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) expression via an m6A-YTHDF2-dependent manner and KCNQ1OT1 could directly bind to Homeobox A9 (HOXA9) to further regulate the proliferation, invasion and metastasis of laryngeal squamous cell carcinoma cells.
Responsed Disease Laryngeal cancer ICD-11: 2C23
Cell Process Cell proliferation
Cell migration
Cell invasion
In-vitro Model
HOK Normal Hexagrammos otakii CVCL_YE19
Tu 212 Head and neck squamous cell carcinoma Homo sapiens CVCL_4915
AMC-HN-8 Laryngeal squamous cell carcinoma Homo sapiens CVCL_5966
In-vivo Model 1 × 106 (100 ul) cells of infected and uninfected by lentiviral were, respectively, injected subcutaneously into nude mice which divided randomly into scramble group and shKCNQ1OT1-1 group.
References
Ref 1 ALKBH5-mediated m6A modification of lncRNA KCNQ1OT1 triggers the development of LSCC via upregulation of HOXA9. J Cell Mol Med. 2022 Jan;26(2):385-398. doi: 10.1111/jcmm.17091. Epub 2021 Dec 1.