Dysregulation of the basal RNA polymerase transcription apparatus in cancer

被引:197
作者
Bywater, Megan J. [1 ,2 ]
Pearson, Richard B. [1 ,2 ,3 ,4 ]
McArthur, Grant A. [1 ,3 ,5 ,6 ]
Hannan, Ross D. [1 ,2 ,3 ,4 ,7 ]
机构
[1] Peter MacCallum Canc Ctr, Div Canc Res, Melbourne, Vic 8006, Australia
[2] Univ Melbourne, Sir Peter MacCallum Dept Oncol, Parkville, Vic 3010, Australia
[3] Univ Melbourne, Dept Biochem & Mol Biol, Parkville, Vic 3010, Australia
[4] Monash Univ, Dept Biochem & Mol Biol, Clayton, Vic 3800, Australia
[5] Univ Melbourne, Dept Med, St Vincents Hosp, Fitzroy, Vic 3065, Australia
[6] Peter MacCallum Canc Ctr, Div Canc Med, Melbourne, Vic 8006, Australia
[7] Univ Queensland, Sch Biomed Sci, Brisbane, Qld 4072, Australia
基金
澳大利亚国家健康与医学研究理事会; 英国医学研究理事会;
关键词
TATA-BINDING PROTEIN; ELONGATION COMPLEX SEC; C-MYC; III TRANSCRIPTION; MEDIATOR COMPLEX; I TRANSCRIPTION; RIBOSOME BIOGENESIS; COACTIVATOR COMPLEX; NONCODING RNAS; POL-II;
D O I
10.1038/nrc3496
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Mutations that directly affect transcription by RNA polymerases rank among the most central mediators of malignant transformation, but the frequency of new anticancer drugs that selectively target defective transcription apparatus entering the clinic has been limited. This is because targeting the large protein-protein and protein-DNA interfaces that control both generic and selective aspects of RNA polymerase transcription has proved extremely difficult. However, recent technological advances have led to a 'quantum leap' in our comprehension of the structure and function of the core RNA polymerase components, how they are dysregulated in a broad range of cancers and how they may be targeted for 'transcription therapy'.
引用
收藏
页码:299 / 314
页数:16
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