Methyltransferase-like proteins in cancer biology and potential therapeutic targeting.


Journal

Journal of hematology & oncology
ISSN: 1756-8722
Titre abrégé: J Hematol Oncol
Pays: England
ID NLM: 101468937

Informations de publication

Date de publication:
02 08 2023
Historique:
received: 10 03 2023
accepted: 10 07 2023
medline: 4 8 2023
pubmed: 3 8 2023
entrez: 2 8 2023
Statut: epublish

Résumé

RNA modification has recently become a significant process of gene regulation, and the methyltransferase-like (METTL) family of proteins plays a critical role in RNA modification, methylating various types of RNAs, including mRNA, tRNA, microRNA, rRNA, and mitochondrial RNAs. METTL proteins consist of a unique seven-beta-strand domain, which binds to the methyl donor SAM to catalyze methyl transfer. The most typical family member METTL3/METTL14 forms a methyltransferase complex involved in N6-methyladenosine (m6A) modification of RNA, regulating tumor proliferation, metastasis and invasion, immunotherapy resistance, and metabolic reprogramming of tumor cells. METTL1, METTL4, METTL5, and METTL16 have also been recently identified to have some regulatory ability in tumorigenesis, and the rest of the METTL family members rely on their methyltransferase activity for methylation of different nucleotides, proteins, and small molecules, which regulate translation and affect processes such as cell differentiation and development. Herein, we summarize the literature on METTLs in the last three years to elucidate their roles in human cancers and provide a theoretical basis for their future use as potential therapeutic targets.

Identifiants

pubmed: 37533128
doi: 10.1186/s13045-023-01477-7
pii: 10.1186/s13045-023-01477-7
pmc: PMC10394802
doi:

Substances chimiques

Methyltransferases EC 2.1.1.-
Adenosine K72T3FS567
MicroRNAs 0
METTL3 protein, human EC 2.1.1.62
METTL16 protein, human EC 2.1.1.-

Types de publication

Journal Article Review Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

89

Informations de copyright

© 2023. The Author(s).

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pubmed: 32576970
Nucleic Acids Res. 2021 Jul 21;49(13):7239-7255
pubmed: 34023900
Theranostics. 2020 Apr 27;10(13):5671-5686
pubmed: 32483411
Cell Death Dis. 2021 Sep 24;12(10):870
pubmed: 34561421
Aging Cell. 2021 Feb;20(2):e13298
pubmed: 33440070
Signal Transduct Target Ther. 2021 Feb 27;6(1):89
pubmed: 33637677

Auteurs

Ya-Nan Qi (YN)

Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450052, P.R. China.

Zhu Liu (Z)

Zhejiang Cancer Institute, Zhejiang Cancer Hospital, No.1 Banshan East Rd., Gongshu District, Hangzhou, 310022, Zhejiang, P.R. China.
Hangzhou Institute of Medicine (HIM), Chinese Academy of Sciences, Hangzhou, 310018, Zhejiang, P.R. China.

Lian-Lian Hong (LL)

Zhejiang Cancer Institute, Zhejiang Cancer Hospital, No.1 Banshan East Rd., Gongshu District, Hangzhou, 310022, Zhejiang, P.R. China.
Hangzhou Institute of Medicine (HIM), Chinese Academy of Sciences, Hangzhou, 310018, Zhejiang, P.R. China.

Pei Li (P)

Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450052, P.R. China. lipeifreemai@zzu.edu.cn.

Zhi-Qiang Ling (ZQ)

Zhejiang Cancer Institute, Zhejiang Cancer Hospital, No.1 Banshan East Rd., Gongshu District, Hangzhou, 310022, Zhejiang, P.R. China. lingzq@zjcc.org.cn.
Hangzhou Institute of Medicine (HIM), Chinese Academy of Sciences, Hangzhou, 310018, Zhejiang, P.R. China. lingzq@zjcc.org.cn.

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