Breaking news: high-speed race ends in arrest - how oncogenes induce senescence

被引:59
作者
Di Micco, Raffaella [1 ]
Fumagalli, Marzia [1 ]
di Fagagna, Fabrizio d'Adda [1 ]
机构
[1] FIRC Inst Mol Oncol Fdn, IOFM Fdn, I-20139 Milan, Italy
关键词
D O I
10.1016/j.tcb.2007.07.012
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Oncogene activation in normal cells induces a permanent proliferative arrest known as cellular senescence. This phenomenon restrains the expansion of cells that bear an activated oncogene and acts as a powerful tumor-suppressive process. Although the full molecular mechanisms are still being elucidated, it has been observed recently that some oncogenes alter the DNA-replication process and cause DNA-damage accumulation. DNA-damage checkpoint-response activation together with the increased appearance of heterochromatin formation that leads to transcriptional silencing of proliferative genes are, presently, the two main mechanisms known that establish and maintain oncogene-induced senescence. Here, we discuss the most recent advancements in understanding the molecular and cellular mechanisms that control cellular senescence caused by oncogene activation and their impact on cancer studies.
引用
收藏
页码:529 / 536
页数:8
相关论文
共 84 条
[21]   Deregulated replication licensing causes DNA fragmentation consistent with head-to-tail fork collision [J].
Davidson, Iain F. ;
Li, Anatoliy ;
Blow, J. Julian .
MOLECULAR CELL, 2006, 24 (03) :433-443
[22]   Rac1 GTPase regulates cell genomic stability and senescence [J].
Debidda, Marcella ;
Williams, David A. ;
Zheng, Yi .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2006, 281 (50) :38519-38528
[23]   Deregulated E2F activity induces hyperplasia and senescence-like features in the mouse pituitary gland [J].
Denchi, EL ;
Attwooll, C ;
Pasini, D ;
Helin, K .
MOLECULAR AND CELLULAR BIOLOGY, 2005, 25 (07) :2660-2672
[24]   Oncogene-induced senescence is a DNA damage response triggered by DNA hyper-replication [J].
Di Micco, Raffaella ;
Fumagalli, Marzia ;
Cicalese, Angelo ;
Piccinin, Sara ;
Gasparini, Patrizia ;
Luise, Chiara ;
Schurra, Catherine ;
Garre, Massimiliano ;
Nuciforo, Paolo Giovanni ;
Bensimon, Aaron ;
Maestro, Roberta ;
Pelicci, Pier Giuseppe ;
di Fagagna, Fabrizio d'Adda .
NATURE, 2006, 444 (7119) :638-642
[25]   A BIOMARKER THAT IDENTIFIES SENESCENT HUMAN-CELLS IN CULTURE AND IN AGING SKIN IN-VIVO [J].
DIMRI, GP ;
LEE, XH ;
BASILE, G ;
ACOSTA, M ;
SCOTT, C ;
ROSKELLEY, C ;
MEDRANO, EE ;
LINSKENS, M ;
RUBELJ, I ;
PEREIRASMITH, O ;
PEACOCKE, M ;
CAMPISI, J .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (20) :9363-9367
[26]   Abnormality of the DNA double-strand-break checkpoint/repair genes, ATM, BRCA1 and TP53, in breast cancer is related to tumour grade [J].
Ding, SL ;
Sheu, LF ;
Yu, JC ;
Yang, TL ;
Chen, BF ;
Leu, FJ ;
Shen, CY .
BRITISH JOURNAL OF CANCER, 2004, 90 (10) :1995-2001
[27]   53BP1 functions in an ATM-dependent checkpoint pathway that is constitutively activated in human cancer [J].
DiTullio, RA ;
Mochan, TA ;
Venere, M ;
Bartkova, J ;
Sehested, M ;
Bartek, J ;
Halazonetis, TD .
NATURE CELL BIOLOGY, 2002, 4 (12) :998-1002
[28]   Non-transcriptional control of DNA replication by c-Myc [J].
Dominguez-Sola, David ;
Ying, Carol Y. ;
Grandori, Carla ;
Ruggiero, Luca ;
Chen, Brenden ;
Li, Muyang ;
Galloway, Denise A. ;
Gu, Wei ;
Gautier, Jean ;
Dalla-Favera, Riccardo .
NATURE, 2007, 448 (7152) :445-U3
[29]   p14ARF activates a Tip60-dependent and p53-independent ATM/ATR/CHK pathway in response to genotoxic stress [J].
Eymin, Beatrice ;
Claverie, Paule ;
Salon, Caroline ;
Leduc, Camille ;
Col, Edwige ;
Brambilla, Elisabeth ;
Khochbin, Saadi ;
Gazzeri, Sylvie .
MOLECULAR AND CELLULAR BIOLOGY, 2006, 26 (11) :4339-4350
[30]   Loss of linker histone H1 in cellular senescence [J].
Funayama, Ryo ;
Saito, Motoki ;
Tanobe, Hiroko ;
Ishikawa, Fuyuki .
JOURNAL OF CELL BIOLOGY, 2006, 175 (06) :869-880