m6A-centered Crosstalk Information

Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT00181
 [1], [2], [3], [4]
m6A modification ADAR1 ADAR1 METTL3 Methylation : m6A sites Direct Enhancement RNA modification MYC MYC ADAR Methylation : modification sites
m6A Modification:
m6A Regulator Methyltransferase-like 3 (METTL3) WRITER
 Regulator Info 
m6A Target Interferon-inducible protein 4 (ADAR1)
 Targert Gene 
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type RNA modification (RNAMod)  >> Adenosine-to-Inosine editing (A-to-I)
Epigenetic Regulator Interferon-inducible protein 4 (ADAR1) WRITER View Details
Regulated Target Myc proto-oncogene protein (MYC) View Details
Crosstalk Relationship m6A  →  A-to-I Enhancement
Crosstalk Mechanism m6A modification directly impacts RNA modification through modulating the expression level of RNA modification regulator
Crosstalk Summary METTL3 methylates Interferon-inducible protein 4 (ADAR1) mRNA, thereby enhancing its protein expression, which subsequently promotes ADAR mediated A-to-I RNA editing of the Myc proto-oncogene protein (MYC) transcript.
Responsed Drug AVI-5126
 Drug Info 
Pathway Response mRNA surveillance pathway hsa03015
RNA degradation hsa03018
Cell Process RNA stability
In-vitro Model
 MGG8 Glioblastoma Homo sapiens CVCL_D1H4
U-87MG ATCC Glioblastoma Homo sapiens CVCL_0022
U-118MG Astrocytoma Homo sapiens CVCL_0633
K-562 Chronic myelogenous leukemia Homo sapiens CVCL_0004
PANC-1 Pancreatic ductal adenocarcinoma Homo sapiens CVCL_0480
BxPC-3 Pancreatic ductal adenocarcinoma Homo sapiens CVCL_0186
Full List of Potential Compound(s) Related to This m6A-centered Crosstalk
Myc proto-oncogene protein (MYC) 3 Compound(s) Regulating the Target Click to Show/Hide the Full List
 Compound Name AVI-5126 Phase 2 [5]
Synonyms
Resten-CP; NeuGene (CABG), AVI
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External Link
TTD: D01VDI
 Compound Name Resten-NG Phase 2 [6]
Synonyms
Resten-NG (TN)
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External Link
TTD: D0M4MG
 Compound Name TWS-119 Investigative [7]
Synonyms
TWS119; 601514-19-6; 3-[[6-(3-Aminophenyl)-7H-pyrrolo[2,3-d]pyrimidin-4-yl]oxy]phenol; TWS 119; GSK inhibitor XII; GSK-3beta Inhibitor XII, TWS119; Neurogenesis Inducer, TWS119; CHEMBL405759; 3-(6-(3-aminophenyl)-7H-pyrrolo[2,3-d]pyrimidin-4-yloxy)phenol; 3-((6-(3-AMINOPHENYL)-7H-PYRROLO[2,3-D]PYRIMIDIN-4-YL)OXY)PHENOL; 3-{[6-(3-aminophenyl)-7H-pyrrolo[2,3-d]pyrimidin-4-yl]oxy}phenol; Phenol, 3-[[6-(3-aminophenyl)-1H-pyrrolo[2,3-d]pyrimidin-4-yl]oxy]-; K00245; MLS006011018; GTPL5980; SCHEMBL5559045; GSK-3BETA INHIB
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External Link
CID: 9549289
TTD: D0T8KR
References
Ref 1 N?-Methyladenosine Landscape of Glioma Stem-Like Cells: METTL3 Is Essential for the Expression of Actively Transcribed Genes and Sustenance of the Oncogenic Signaling. Genes (Basel). 2019 Feb 13;10(2):141. doi: 10.3390/genes10020141.
Ref 2 ADAR1 is a new target of METTL3 and plays a pro-oncogenic role in glioblastoma by an editing-independent mechanism. Genome Biol. 2021 Jan 28;22(1):51. doi: 10.1186/s13059-021-02271-9.
Ref 3 ADAR1 may be involved in the proliferation of acute myeloid leukemia cells via regulation of the Wnt pathway. Cancer Manag Res. 2019 Sep 20;11:8547-8555. doi: 10.2147/CMAR.S210504. eCollection 2019.
Ref 4 The aberrant expression of ADAR1 promotes resistance to BET inhibitors in pancreatic cancer by stabilizing c-Myc. Am J Cancer Res. 2020 Jan 1;10(1):148-163. eCollection 2020.
Ref 5 Efficacy of a phosphorodiamidate morpholino oligomer antisense compound in the inhibition of corneal transplant rejection in a rat cornea transplant model. J Ocul Pharmacol Ther. 2012 Apr;28(2):194-201. doi: 10.1089/jop.2011.0135. Epub 2011 Dec 7.
Ref 6 Local delivery of c-myc neutrally charged antisense oligonucleotides with transport catheter inhibits myointimal hyperplasia and positively affects vascular remodeling in the rabbit balloon injury model. Catheter Cardiovasc Interv. 2001 Oct;54(2):247-56. doi: 10.1002/ccd.1277.
Ref 7 TTD: Therapeutic Target Database describing target druggability information. Nucleic Acids Res. 2024 Jan 5;52(D1):D1465-D1477. doi: 10.1093/nar/gkad751.