Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT05871
[1]
m6A modification Lnc668 Lnc668 YTHDC1 : m6A sites Direct Enhancement Non-coding RNA lnc668 PICALM  lncRNA       miRNA   circRNA
m6A Modification:
m6A Regulator YTH domain-containing protein 1 (YTHDC1) READER
m6A Target Lnc668
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type Non-coding RNA (ncRNA)
Epigenetic Regulator Lnc668 LncRNA View Details
Regulated Target Phosphatidylinositol-binding clathrin assembly protein (PICALM) View Details
Crosstalk Relationship m6A  →  ncRNA Enhancement
Crosstalk Mechanism m6A regulators directly modulate the functionality of ncRNAs through specific targeting ncRNA
Crosstalk Summary The m6A reader YTHDC1 recognized m6A-modified Lnc668 and elevated the METTL3-mediated lnc668 modification. lnc668 enhanced Phosphatidylinositol-binding clathrin assembly protein (PICALM) mRNA stability to promote pulmonary fibrogenesis depending on YTHDC1 phase separation
Responsed Disease Pulmonary fibrosis ICD-11: CA60
Cell Process Cell differentiation
In-vitro Model
MRC-5 Normal Homo sapiens CVCL_0440
In-vivo Model Eight-week-old C57BL/6 mice were provided by Jinan Pengyue Company and divided into the following groups according to experimental requirements: sham operation group, BLM model group, BLM + si-lnc668/NC group, BLM + si-lnc668 group, overexpressed lnc668/NC group, and overexpressed lnc668 treatment group, with 10 mice in each group. Anesthesia was induced by intraperitoneal injection of 4% chloral hydrate (10 mg/kg). The sham operation group received an equivalent volume of saline as a control.
References
Ref 1 YTHDC1 phase separation drives the nuclear export of m(6)A-modified lncNONMMUT062668.2 through the transport complex SRSF3-ALYREF-XPO5 to aggravate pulmonary fibrosis. Cell Death Dis. 2025 Apr 12;16(1):279. doi: 10.1038/s41419-025-07608-x.