Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT05364
[1]
Non-coding RNA LINC00470 METTL3  lncRNA       miRNA   circRNA Direct Enhancement m6A modification PTEN PTEN METTL3 Methylation : m6A sites
m6A Modification:
m6A Regulator Methyltransferase-like 3 (METTL3) WRITER
m6A Target Mutated in multiple advanced cancers 1 (PTEN)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type Non-coding RNA (ncRNA)
Epigenetic Regulator Long intergenic non-protein coding RNA 470 (LINC00470) LncRNA View Details
Regulated Target Methyltransferase-like protein 3 (METTL3) View Details
Crosstalk Relationship ncRNA  →  m6A Enhancement
Crosstalk Mechanism ncRNAs directly impacts m6A modification through recruiting m6A regulator
Crosstalk Summary Our results demonstrated the molecular mechanism underlying the effect of LINC00470 on CML by reducing the Mutated in multiple advanced cancers 1 (PTEN) stability via RNA methyltransferase METTL3, thus leading to the inhibition of cell autophagy while promoting chemoresistance in CML.
Responsed Disease Chronic myeloid leukaemia ICD-11: 2B33.2
Pathway Response Autophagy hsa04140
Cell Process RNA stability
Cell autophagy
References
Ref 1 Dysregulation of LINC00470 and METTL3 promotes chemoresistance and suppresses autophagy of chronic myelocytic leukaemia cells. J Cell Mol Med. 2021 May;25(9):4248-4259. doi: 10.1111/jcmm.16478. Epub 2021 Mar 21.