scholarly journals The DNA damage signaling pathway is a critical mediator of oncogene-induced senescence

2007 ◽  
Vol 21 (1) ◽  
pp. 43-48 ◽  
Author(s):  
F. A. Mallette ◽  
M.-F. Gaumont-Leclerc ◽  
G. Ferbeyre
2012 ◽  
Vol 52 (6) ◽  
pp. 311-317 ◽  
Author(s):  
Kaisar A. Talukder ◽  
Ishrat J. Azmi ◽  
K. Ahtesham Ahmed ◽  
M. Sabir Hossain ◽  
Yearul Kabir ◽  
...  

2012 ◽  
Vol 83 (6) ◽  
pp. 747-757 ◽  
Author(s):  
Jung-Hoon Yoon ◽  
Sang-Gun Ahn ◽  
Byung-Hoon Lee ◽  
Sung-Hoo Jung ◽  
Seon-Hee Oh

2014 ◽  
Vol 70 (6) ◽  
pp. 701-713 ◽  
Author(s):  
Ran Gao ◽  
Rumani Singh ◽  
Zeenia Kaul ◽  
Sunil C. Kaul ◽  
Renu Wadhwa

2015 ◽  
Vol 10 (3) ◽  
pp. 1769-1774 ◽  
Author(s):  
CHAO SUN ◽  
ZHONGYONG WANG ◽  
WUCHAO SONG ◽  
BAOMIN CHEN ◽  
JINSHI ZHANG ◽  
...  

2007 ◽  
Vol 83 (1) ◽  
pp. 9-15 ◽  
Author(s):  
Huda H. Al-Khalaf ◽  
Boleslaw Lach ◽  
Ayman Allam ◽  
Ahmed AlKhani ◽  
Salman A. Alrokayan ◽  
...  

Cell Cycle ◽  
2007 ◽  
Vol 6 (15) ◽  
pp. 1831-1836 ◽  
Author(s):  
Frédérick A. Mallette ◽  
Gerardo Ferbeyre

2006 ◽  
Vol 17 (4) ◽  
pp. 1583-1592 ◽  
Author(s):  
Olga Moiseeva ◽  
Frédérick A. Mallette ◽  
Utpal K. Mukhopadhyay ◽  
Adrian Moores ◽  
Gerardo Ferbeyre

Interferons are cytokines with potent antiviral and antiproliferative activities. We report that although a transient exposure to β-interferon induces a reversible cell cycle arrest, a sustained treatment triggers a p53-dependent senescence program. β-Interferon switched on p53 in two steps. First, it induced the acetylation of p53 at lysine 320 and its dephosphorylation at serine 392 but not p53 activity. Later on, it triggered a DNA signaling pathway, the phosphorylation of p53 at serine 15 and its transcriptional activity. In agreement, β-interferon–treated cells accumulated γ-H2AX foci and phosphorylated forms of ATM and CHK2. The DNA damage signaling pathway was activated by an increase in reactive oxygen species (ROS) induced by interferon and was inhibited by the antioxidant N-acetyl cysteine. More important, RNA interference against ATM inhibited p53 phosphorylation at serine 15, p53 activity and senescence in response to β-interferon. β-Interferon–induced senescence was more efficient in cells expressing either, p53, or constitutive allele of ERK2 or RasV12. Hence, β-interferon–induced senescence targets preferentially cells with premalignant changes.


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