@Article{ecn.2007.0106,
AUTHOR = {René Rodríguez, Victor M. Campa, José Riera, M. Teresa Carcedo, David S. Ucker, Sofía Ramos, Pedro S. Lazo},
TITLE = {TNF triggers mitogenic signals in NIH 3T3 cells but induces apoptosis when the cell cycle is blocked},
JOURNAL = {European Cytokine Network},
VOLUME = {18},
YEAR = {2007},
NUMBER = {4},
PAGES = {172--180},
URL = {http://www.techscience.com/ECN/v18n4/65967},
ISSN = {1952-4005},
ABSTRACT = {Tumor necrosis factor (TNF) is known to be a mediator of a variety of cellular responses including
apoptotic death or proliferation depending on the target cell and the environmental conditions. We show here that
TNF triggers both growth and death signals in NIH 3T3 murine fibroblasts. In cells arrested in G<sub>0</sub> by serum
deprivation, TNF drives approximately 50% of them to enter the cell cycle, but kills the cells that remain
quiescent. The presence of serum prevents toxic effects of TNF, suggesting that TNF can cooperate to drive cells
through the cell cycle, but is unable to do so by itself and alternatively it triggers death signals in cells unable to
proliferate. Interestingly, TNF induces a similar toxic effect in cells forced to stay at the G<sub>01</sub>
 /S border, S or M
phases. We have explored the TNF apoptotic pathway in arrested cells. This mechanism is not due to the loss of
the anti-apoptotic capacity of NFκB and is mediated by mitochondria since Bcl-2 overexpression partially inhibits
cell death. There are, however, interesting differences in the kinetics of mitochondrial events which indicate that
this form of sensitization to TNF leads to an apoptotic mechanism different from that observed after sensitization
by RNA synthesis inhibition.},
DOI = {10.1684/ecn.2007.0106}
}