Critical Roles of METTL3 in Translation Regulation of Cancer

被引:9
|
作者
Meng, Wangyang [1 ,2 ]
Xiao, Han [1 ]
Mei, Peiyuan [1 ]
Chen, Jiaping [1 ]
Wang, Yangwei [1 ]
Zhao, Rong [1 ]
Liao, Yongde [1 ]
机构
[1] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Thorac Surg, Wuhan 430022, Peoples R China
[2] Shanghai Jiao Tong Univ, Ruijin Hosp, Sch Med, Dept Thorac Surg, Shanghai 200000, Peoples R China
基金
中国国家自然科学基金;
关键词
METTL3; m(6)A; translation regulation; post-transcriptional modification; eukaryotic initiation factor; RNA binding protein; cancer; MESSENGER-RNA; M(6)A METHYLATION; SUBUNIT; EXPRESSION; GENE; BREAST; EIF4E; TUMORIGENESIS; AMPLIFICATION; CLONING;
D O I
10.3390/biom13020243
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Aberrant translation, a characteristic feature of cancer, is regulated by the complex and sophisticated RNA binding proteins (RBPs) in the canonical translation machinery. N6-methyladenosine (m(6)A) modifications are the most abundant internal modifications in mRNAs mediated by methyltransferase-like 3 (METTL3). METTL3 is commonly aberrantly expressed in different tumors and affects the mRNA translation of many oncogenes or dysregulated tumor suppressor genes in a variety of ways. In this review, we discuss the critical roles of METTL3 in translation regulation and how METTL3 and m(6)A reader proteins in collaboration with RBPs within the canonical translation machinery promote aberrant translation in tumorigenesis, providing an overview of recent efforts aiming to 'translate' these results to the clinic.
引用
收藏
页数:14
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