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By Blocking Apoptosis, Bcl-2 in p38-Dependent Manner Promotes Cell Cycle Arrest and Accelerated Senescence After DNA Damage and Serum Withdrawal
Anna Nelyudova, Nikolay Aksenov, Valery Pospelov and Tatiana Pospelova
volume 6 | issue 17
1 September 2007Pages: 2171 - 2177
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E1A+ras-transformed rodent fibroblasts are unable to be arrested in the cell cycle and die by apoptosis in response to cytostatics, ionizing radiation (IR), or serum withdrawal. Overexpression of the human antiapoptotic gene bcl-2 suppresses apoptosis and induces reversible cell cycle arrest after IR or serum withdrawal and cell senescence after adriamycin treatment. Bcl-2-sustained adriamycin-induced cell senescence requires p38 MAPK, since the knockout of p38 MAPK abrogated anti-apoptotic and senescence-inducing effects of Bcl-2 in adriamycin-treated cells. Moreover, resistance to apoptosis and cell cycle arrest were not observed in p38 -/- E1A+ras+bcl-2-transformants following IR or serum deprivation. However, the pro-apoptotic effect of nocodazole in E1A+ras-transformed cells can not be prevented by Bcl-2 overexpression independently of the presence of p38 MAPK. These results allow us to conclude that p38 is necessary for Bcl-2-induced inhibition of apoptosis, induction of cell cycle arrest and accelerated senescence after DNA damage and serum starvation, but not after nocodazole treatment.
Authors
Anna Nelyudova
Russian Academy of Sciences; St. Petersburg, Russia
Nikolay Aksenov
Russian Academy of Sciences; St. Petersburg, Russia
Valery Pospelov
Russian Academy of Sciences; St. Petersburg, Russia
Tatiana Pospelova
Russian Academy of Sciences; St. Petersburg, Russia
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.