p73:: A chiaroscuro gene in cancer

被引:35
作者
Marabese, Mirko [1 ]
Vikhanskaya, Faina [1 ]
Broggini, Massimo [1 ]
机构
[1] Ist Ric Farmacol Mario Negri, Mol Pharmacol Lab, I-20157 Milan, Italy
关键词
p73; p53; family; transcriptional regulation; post-transcriptional modification; cancer; DNp73; anticancer drugs; mutants;
D O I
10.1016/j.ejca.2007.01.042
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
p73 is a member of the p53 family which is gaining increasing importance in the field of cancer. Its structural homology with p53 led to the assumption that it could act as a new tumour suppressor gene. Increasing knowledge of its function, however, has cast doubts on this role. A particularly interesting characteristic of p73 is that the cell contains different isoforms with distinct and sometimes opposite functions. Evidence in the last few years clearly indicates that p73 does share some activities with p53 but also that it has some distinct functions. This review focuses on p73's role in the development and progression of cancer, analysing the gene structure and regulation and discussing similarities with p53 and differences. Recent results obtained with specific detection methods on the levels and functions of the different isoforms in tumours are also discussed. (C) 2007 Elsevier Ltd. All rights reserved.
引用
收藏
页码:1361 / 1372
页数:12
相关论文
共 95 条
[1]  
Agami R, 1999, NATURE, V399, P809
[2]   Human cytomegalovirus induces drug resistance and alteration of programmed cell death by accumulation of ΔN-p73α [J].
Allart, S ;
Martin, H ;
Détraves, C ;
Terrasson, J ;
Caput, D ;
Davrinche, C .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (32) :29063-29068
[3]   A mechanism of ubiquitin-independent proteasomal degradation of the tumor suppressors p53 and p73 [J].
Asher, G ;
Tsvetkov, P ;
Kahana, C ;
Shaul, Y .
GENES & DEVELOPMENT, 2005, 19 (03) :316-321
[4]   Induction of p57KIP2 expression by p73β [J].
Bálint, É ;
Phillips, AC ;
Kozlov, S ;
Stewart, CL ;
Vousden, KH .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (06) :3529-3534
[5]   ASPP1 and ASPP2: Common activators of p53 family members [J].
Bergamaschi, D ;
Samuels, Y ;
Jin, BQ ;
Duraisingham, S ;
Crook, T ;
Lu, X .
MOLECULAR AND CELLULAR BIOLOGY, 2004, 24 (03) :1341-1350
[6]   p53 polymorphism influences response in cancer chemotherapy via modulation of p73-dependent apoptosis [J].
Bergamaschi, D ;
Gasco, M ;
Hiller, L ;
Sullivan, A ;
Syed, N ;
Trigiante, G ;
Yulug, I ;
Merlano, M ;
Numico, G ;
Comino, A ;
Attard, M ;
Reelfs, O ;
Gusterson, B ;
Bell, AK ;
Heath, V ;
Tavassoli, M ;
Farrell, PJ ;
Smith, P ;
Lu, X ;
Crook, T .
CANCER CELL, 2003, 3 (04) :387-402
[7]   Ubiquitin-dependent degradation of p73 is inhibited by PML [J].
Bernassola, F ;
Salomoni, P ;
Oberst, A ;
Di Como, CJ ;
Pagano, M ;
Melino, G ;
Pandolfi, PP .
JOURNAL OF EXPERIMENTAL MEDICINE, 2004, 199 (11) :1545-1557
[8]   p53 isoforms can regulate p53 transcriptional activity [J].
Bourdon, JC ;
Fernandes, K ;
Murray-Zmijewski, F ;
Liu, G ;
Diot, A ;
Xirodimas, DP ;
Saville, MK ;
Lane, DP .
GENES & DEVELOPMENT, 2005, 19 (18) :2122-2137
[9]   p73 is transcriptionally regulated by DNA damage, p53, and p73 [J].
Chen, XB ;
Zheng, YM ;
Zhu, JH ;
Jiang, JY ;
Wang, J .
ONCOGENE, 2001, 20 (06) :769-774
[10]   Transdominant ΔTAp73 isoforms are frequently up-regulated in ovarian cancer.: Evidence for their role as epigenetic p53 inhibitors in vivo [J].
Concin, N ;
Becker, K ;
Slade, N ;
Erster, S ;
Mueller-Holzner, E ;
Ulmer, H ;
Daxenbichler, G ;
Zeimet, A ;
Zeillinger, R ;
Marth, C ;
Moll, UM .
CANCER RESEARCH, 2004, 64 (07) :2449-2460