p53 as the main traffic controller of the cell signaling network

被引:13
作者
Sebastian, Sinto [1 ]
Azzariti, Amalia [1 ]
Silvestris, Nicola [2 ]
Porcelli, Letizia [1 ]
Russo, Antonio [3 ]
Tommasino, Massimo [4 ]
Paradiso, Angelo [1 ]
机构
[1] Natl Canc Inst Giovanni Paolo 2, Clin Expt Oncol Lab, I-70126 Bari, Italy
[2] Natl Canc Inst Giovanni Paolo 2, Med & Expt Oncol Unit, I-70126 Bari, Italy
[3] Univ Palermo, Sect Med Oncol, Dept Surg & Oncol, Palermo, Italy
[4] Int Agcy Res Canc, Infect & Canc Biol Grp, F-69372 Lyon 8, France
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2010年 / 15卷
关键词
Cancer; p53; Cell Signaling; Apoptosis; Cell Cycle; Review; HUMAN-PAPILLOMAVIRUS TYPE-16; TUMOR-SUPPRESSOR P53; ONCOGENE-INDUCED SENESCENCE; FACTOR-BINDING-SITES; DNA-DAMAGE RESPONSE; C-TERMINAL DOMAIN; WILD-TYPE P53; TRANSCRIPTIONAL REPRESSION; P53-DEPENDENT APOPTOSIS; GENE-EXPRESSION;
D O I
10.2741/3669
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
Among different pathological conditions that affect human beings, cancer has received a great deal of attention primarily because it leads to significant morbidity and mortality. This is essetnially due to increasing worldwide incidence of this disease and the inability to discover the cause and molecular mechanisms by which normal human cells acquire the characteristics that define cancer cells. Since the discovery of p53 over a quarter of a century ago, it is now recognized that virtually all cell fate pathways of live cells and the decision to die are under the control of p53. Such extensive involvement indicates that p53 protein is acting as a major traffic controller in the cell signaling network. In cancer cells, many cell signaling pathways of normal human cells are rerouted towards immortalization and this is accomplished by the corruption of the main controllers of cell signaling pathways such as p53. This review highlights how p53 signaling activity is altered in cancer cells so that cells acquire the hallmarks of cancer including deregulated infinite self replicative potential.
引用
收藏
页码:1172 / 1190
页数:19
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