Epigenetic silencing of 14-3-3sigma in cancer

被引:58
作者
Lodygin, Dmitri [1 ]
Hermeking, Heiko [1 ]
机构
[1] Max Planck Inst Biochem, Independent Max Planck Res Grp, D-82152 Munich, Germany
关键词
14-3-3; sigma; cell cycle; CpG methylation; p53; cancer; 14-3-3sigma;
D O I
10.1016/j.semcancer.2006.03.008
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The 14-3-3 sigma gene is a direct target of the p53 tumor suppressor and its product inhibits cell cycle progression. Recently, a proteomic analysis revealed that 14-3-3 sigma regulates additional cellular processes relevant to carcinogenesis, as migration and MAP-kinase signalling. The expression of 14-3-3o- is down-regulated by CpG methylation in several types of human cancer, among them prostate, lung, breast and several types of skin cancer. The epigenetic inactivation of 14-3-3 sigma occurs at an early stage of tumor development and may allow evasion from senescence and promote genomic instability. In the future the detection of CpG methylation of 14-3-3 sigma may be used for diagnostic and prognostic purposes. (c) 2006 Elsevier Ltd. All rights reserved.
引用
收藏
页码:214 / 224
页数:11
相关论文
共 113 条
[11]   DNA methylation patterns and epigenetic memory [J].
Bird, A .
GENES & DEVELOPMENT, 2002, 16 (01) :6-21
[12]   Myc represses transcription through recruitment of DNA methyltransferase corepressor [J].
Brenner, C ;
Deplus, R ;
Didelot, C ;
Loriot, A ;
Viré, E ;
De Smet, C ;
Gutierrez, A ;
Danovi, D ;
Bernard, D ;
Boon, T ;
Pelicci, PG ;
Amati, B ;
Kouzarides, T ;
de Launoit, Y ;
Di Croce, L ;
Fuks, F .
EMBO JOURNAL, 2005, 24 (02) :336-346
[13]   14-3-3σ is required to prevent mitotic catastrophe after DNA damage [J].
Chan, TA ;
Hermeking, H ;
Lengauer, C ;
Kinzler, KW ;
Vogelstein, B .
NATURE, 1999, 401 (6753) :616-620
[14]  
Chan TA, 2000, GENE DEV, V14, P1584
[15]   Crucial role of p53-dependent cellular senescence in suppression of Pten-deficient tumorigenesis [J].
Chen, ZB ;
Trotman, LC ;
Shaffer, D ;
Lin, HK ;
Dotan, ZA ;
Niki, M ;
Koutcher, JA ;
Scher, HI ;
Ludwig, T ;
Gerald, W ;
Cordon-Cardo, C ;
Pandolfi, PP .
NATURE, 2005, 436 (7051) :725-730
[16]   Loss of 14-3-3σ in prostate cancer and its precursors [J].
Cheng, L ;
Pan, CX ;
Zhang, JT ;
Zhang, SB ;
Kinch, MS ;
Li, L ;
Baldridge, LA ;
Wade, C ;
Hu, ZQ ;
Koch, MO ;
Ulbright, TM ;
Eble, JN .
CLINICAL CANCER RESEARCH, 2004, 10 (09) :3064-3068
[17]   Tumour biology -: Senescence in premalignant tumours [J].
Collado, M ;
Gil, J ;
Efeyan, A ;
Guerra, C ;
Schuhmacher, AJ ;
Barradas, M ;
Benguría, A ;
Zaballos, A ;
Flores, JM ;
Barbacid, M ;
Beach, D ;
Serrano, M .
NATURE, 2005, 436 (7051) :642-642
[18]  
De Marzo AM, 1999, CANCER RES, V59, P3855
[19]   Downregulation of 14-3-3σ prevents clonal evolution and leads to immortalization of primary human keratinocytes [J].
Dellambra, E ;
Golisano, O ;
Bondanza, S ;
Siviero, E ;
Lacal, P ;
Molinari, M ;
D'Atri, S ;
De Luca, M .
JOURNAL OF CELL BIOLOGY, 2000, 149 (05) :1117-1129
[20]   Inactivation of 14-3-3σ influences telomere behavior and ionizing radiation-induced chromosomal instability [J].
Dhar, S ;
Squire, JA ;
Hande, MP ;
Wellinger, RJ ;
Pandita, TK .
MOLECULAR AND CELLULAR BIOLOGY, 2000, 20 (20) :7764-7772