Alternative pre-mRNA splicing regulation in cancer: pathways and programs unhinged

被引:632
作者
David, Charles J. [1 ]
Manley, James L. [1 ]
机构
[1] Columbia Univ, Dept Biol Sci, New York, NY 10027 USA
关键词
Alternative splicing; cancer; proliferation; RNA-binding proteins; translation; TRACT-BINDING-PROTEIN; RECEPTOR TYROSINE KINASE; TUMOR-SUPPRESSOR GENE; ENDOTHELIAL GROWTH-FACTOR; INTERNAL RIBOSOME ENTRY; SPINAL MUSCULAR-ATROPHY; CELL-CYCLE PROGRESSION; ANTIGEN-R HUR; HNRNP A1; SR PROTEINS;
D O I
10.1101/gad.1973010
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Alternative splicing of mRNA precursors is a nearly ubiquitous and extremely flexible point of gene control in humans. It provides cells with the opportunity to create protein isoforms of differing, even opposing, functions from a single gene. Cancer cells often take advantage of this flexibility to produce proteins that promote growth and survival. Many of the isoforms produced in this manner are developmentally regulated and are preferentially re-expressed in tumors. Emerging insights into this process indicate that pathways that are frequently deregulated in cancer often play important roles in promoting aberrant splicing, which in turn contributes to all aspects of tumor biology.
引用
收藏
页码:2343 / 2364
页数:22
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