Demethylases in tumors and the tumor microenvironment: Key modifiers of N6-methyladenosine methylation - 27/04/24
, Xiaofeng Jiang c, ⁎ Abstract |
RNA methylation modifications are widespread in eukaryotes and prokaryotes, with N6-methyladenosine (m6A) the most common among them. Demethylases, including Fat mass and obesity associated gene (FTO) and AlkB homolog 5 (ALKBH5), are important in maintaining the balance between RNA methylation and demethylation. Recent studies have clearly shown that demethylases affect the biological functions of tumors by regulating their m6A levels. However, their effects are complicated, and even opposite results have appeared in different articles. Here, we summarize the complex regulatory networks of demethylases, including the most important and common pathways, to clarify the role of demethylases in tumors. In addition, we describe the relationships between demethylases and the tumor microenvironment, and introduce their regulatory mechanisms. Finally, we discuss evaluation of demethylases for tumor diagnosis and prognosis, as well as the clinical application of demethylase inhibitors, providing a strong basis for their large-scale clinical application in the future.
Le texte complet de cet article est disponible en PDF.Graphical Abstract |
The effect of demethylases on tumor progression and their related mechanism. (Created with BioRender.com)
The effect of demethylases on tumor progression and their related mechanism. (Created with BioRender.com)Le texte complet de cet article est disponible en PDF.
Highlights |
• | Demethylases regulate tumor biological functions. |
• | Demethylases can regulate tumor progression by regulating tumor microenvironment(TME). |
• | Demethylases regulate important tumor related pathways. |
Abbreviations : 2OG, AFP, AGO2, ALKBH5, AMD1, AML, APOE, ASB2, ATG-5, ATG7, AUC, AURKB, AXL, BCa, Bcl-2, BMP4, C/EBp-β, CA153, CC, CcRCC, CDK1, CDK2, CDK4, CDKN1Ap21, CDKN2Ap16, CDS, CEA, CELF2, CIDEC, C-jun, CRC, CSCs, DACT1, DCs, DDIT4, DFS, DSBH, DsDNA, EGFR, EIF3a, EIF4G1, EMT, ERCC1, ESCC, F6A, FOS, FOXM1, FTO, G6PD, GBM, GC, GPX4, HCC, HER2, HIF, Hm6A, HNRP, HNSCC, HO-1, HOXB13, HUR, ICC, IFN-γ, IGF2BP, IL-6, IL-8, IRF8, JAK2, JunB, KLF4, L-17ARpL23, LATS2, LDHB, LILRB, LILRB4, LUAD, M1A, M5C, M6A, M6Am, MAPK, Mct4, MDSCs, METTL3, METTL14, METTL16, MIS12, MM, MMP2, MTA1, MXI1, MZF1, NANOG, NEAT1, NFE2L2, NK, NM, NPM1, NSCLC, OC, OCT4, OS, OSCC, OTUB1, PAQR4, PC, PCa, PCNA, PD-1, PDE1C, PDGFC, PDGFRB, PD-L1, PFS, PGC-1a, PPAR-γ, PTC, PTEN, PYCR2, RARA, RCC, REST, RIGi, ROS, SAV1, SDHA, SFPQ, SIRT3, Slc16a3, SLC1A5, SLC3A2, SLC7A11, SMAD3, SMAD6, SOCS, SOD2, Sox10, Sox2, SREBP1c, SsDNA, SsRNA, STAT1, STAT3, TAM, TAZ, TGFβR2, TIAM1, TME, TP53INP2, TRAF1, Tregs, UM, UTR, VEGF, WIF-1, WNT7B, YAP, YTHDF, YTHDF2, ZEB1, ZNF217
Keywords : Cancer, Demethylases, m6A, Molecular mechanism, Therapy, TME
Plan
Vol 174
Article 116479- mai 2024 Retour au numéro
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