通过可变聚腺苷酸化驱动胶质母细胞瘤生长。
Driving glioblastoma growth by alternative polyadenylation.
作者信息
Han Ting, Kim John K
机构信息
Department of Biochemistry, UT Southwestern Medical Center, Dallas, TX 75390-9152, USA.
Life Sciences Institute, Department of Human Genetics, University of Michigan, Ann Arbor, MI 48109-2216, USA.
出版信息
Cell Res. 2014 Sep;24(9):1023-4. doi: 10.1038/cr.2014.88. Epub 2014 Jul 4.
Abstract
Global shortening of 3' untranslated regions (3' UTRs) through alternative polyadenylation is an emerging hallmark of cancer. A recent study identifies the cleavage factor Im 25 (CFIm25) as an important mediator of 3' UTR shortening in glioblastomas and demonstrates a causal relationship between alternative polyadenylation and cancer cell proliferation.
摘要
通过可变聚腺苷酸化导致的3'非翻译区（3'UTR）整体缩短是癌症的一个新特征。最近一项研究确定切割因子Im 25（CFIm25）是胶质母细胞瘤中3'UTR缩短的重要介导因子，并证明了可变聚腺苷酸化与癌细胞增殖之间的因果关系。
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