ETV1, 4 and 5: An oncogenic subfamily of ETS transcription factors

被引:220
作者
Oh, Sangphil [1 ]
Shin, Sook [1 ]
Janknecht, Ralf [1 ]
机构
[1] Univ Oklahoma, Hlth Sci Ctr, Stanton L Young Biomed Res Ctr BRC 1464, Dept Cell Biol, Oklahoma City, OK 73104 USA
来源
BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER | 2012年 / 1826卷 / 01期
关键词
Cancer; Chromosomal translocation; ETS; Posttranslational modification; Transcription factor; ENDOTHELIAL GROWTH-FACTOR; ENHANCER-BINDING-PROTEIN; PROSTATE-CANCER; ANDROGEN RECEPTOR; GENE FUSIONS; FACTOR ER81; UP-REGULATION; TUMOR PROGRESSION; PEA3; SUBFAMILY; BREAST-CANCER;
D O I
10.1016/j.bbcan.2012.02.002
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
The homologous ETV1, ETV4 and ETV5 proteins form the PEA3 subfamily of ETS transcription factors. In Ewing tumors, chromosomal translocations affecting ETV1 or ETV4 are an underlying cause of carcinogenesis. Likewise, chromosomal rearrangements of the ETV1, ETV4 or ETV5 gene occur in prostate tumors and are thought to be one of the major driving forces in the genesis of prostate cancer. In addition, these three ETS proteins are implicated in melanomas, breast and other types of cancer. Complex posttranslational modifications govern the activity of PEA3 factors, which can promote cell proliferation, motility and invasion. Here, we review evidence for a role of ETV1, 4 and 5 as oncoproteins and describe modes of their action. Modulation of their activation or interaction with cofactors as well as inhibiting crucial target gene products may ultimately be exploited to treat various cancers that are dependent on the PEA3 group of ETS transcription factors. (C) 2012 Elsevier B.V. All rights reserved.
引用
收藏
页码:1 / 12
页数:12
相关论文
共 180 条
[1]   Integrating differentiation and cancer:: The Nkx3.1 homeobox gene in prostate organogenesis and carcinogenesis [J].
Abate-Shen, Cory ;
Shen, Michael M. ;
Gelmann, Edward .
DIFFERENTIATION, 2008, 76 (06) :717-727
[2]  
[Anonymous], PATHOLOGY RES INT
[3]   ETS gene Er81 controls the formation of functional connections between group Ia sensory afferents and motor neurons [J].
Arber, S ;
Ladle, DR ;
Lin, JH ;
Frank, E ;
Jessell, TM .
CELL, 2000, 101 (05) :485-498
[4]   Targeting BRAF for patients with melanoma [J].
Arkenau, H-T ;
Kefford, R. ;
Long, G. V. .
BRITISH JOURNAL OF CANCER, 2011, 104 (03) :392-398
[5]   Steroid Hormone Receptors in Prostate Cancer: A Hard Habit to Break? [J].
Attard, Gerhardt ;
Cooper, Colin S. ;
de Bono, Johann S. .
CANCER CELL, 2009, 16 (06) :458-462
[6]   The 26S proteasome system degrades the ERM transcription factor and regulates its transcription-enhancing activity [J].
Baert, J-L ;
Beaudoin, C. ;
Monte, D. ;
Degerny, C. ;
Mauen, S. ;
de Launoit, Y. .
ONCOGENE, 2007, 26 (03) :415-424
[7]   The E3 ubiquitin ligase complex component COP1 regulates PEA3 group member stability and transcriptional activity [J].
Baert, J-L ;
Monte, D. ;
Verreman, K. ;
Degerny, C. ;
Coutte, L. ;
de Launoit, Y. .
ONCOGENE, 2010, 29 (12) :1810-1820
[8]   ERM transactivation is up-regulated by the repression of DNA binding after the PKA phosphorylation of a consensus site at the edge of the ETS domain. [J].
Baert, JL ;
Beaudoin, C ;
Coutte, L ;
de Launoit, Y .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (02) :1002-1012
[9]   Pea3 Transcription Factors and Wnt1-Induced Mouse Mammary Neoplasia [J].
Baker, Rebecca ;
Kent, Claire V. ;
Silbermann, Rachel A. ;
Hassell, John A. ;
Young, Lawrence J. T. ;
Howe, Louise R. .
PLOS ONE, 2010, 5 (01)
[10]   Induction of the SUMO-specific protease 1 transcription by the androgen receptor in prostate cancer cells [J].
Bawa-Khalfe, Tasneem ;
Cheng, Jinke ;
Wang, Zhengxin ;
Yeh, Edward T. H. .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2007, 282 (52) :37341-37349