Regulation of Epithelial-to-Mesenchymal Transition by Alternative Translation Initiation Mechanisms and Its Implications for Cancer Metastasis

被引:17
作者
Bera, Amit [1 ]
Lewis, Stephen M. [1 ,2 ,3 ]
机构
[1] Atlantic Canc Res Inst, Moncton, NB E1C 8X3, Canada
[2] Univ Moncton, Dept Chem & Biochem, Moncton, NB E1A 3E9, Canada
[3] Beatrice Hunter Canc Res Inst, Halifax, NS B3H 4R2, Canada
关键词
epithelial-to-mesenchymal transition (EMT); IRES; m(6)A-mediated translation; ITAF; cancer; metastasis; IRES-MEDIATED TRANSLATION; RIBOSOME ENTRY SITES; MESSENGER-RNA; BREAST-CANCER; LAMININ B1; INTERNAL INITIATION; PROTEIN-SYNTHESIS; MIR-200; FAMILY; ACTING FACTORS; EXPRESSION;
D O I
10.3390/ijms21114075
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
Translation initiation plays a critical role in the regulation of gene expression for development and disease conditions. During the processes of development and disease, cells select specific mRNAs to be translated by controlling the use of diverse translation initiation mechanisms. Cells often switch translation initiation from a cap-dependent to a cap-independent mechanism during epithelial-to-mesenchymal transition (EMT), a process that plays an important role in both development and disease. EMT is involved in tumor metastasis because it leads to cancer cell migration and invasion, and is also associated with chemoresistance. In this review we will provide an overview of both the internal ribosome entry site (IRES)-dependent and N-6-methyladenosine (m(6)A)-mediated translation initiation mechanisms and discuss how cap-independent translation enables cells from primary epithelial tumors to achieve a motile mesenchymal-like phenotype, which in turn drives tumor metastasis.
引用
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页码:1 / 16
页数:16
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