Research Perspectives:

Caspase-2 regulates oncogene-induced senescence

Delphine Gitenay, Hélène Lallet-Daher and David Bernard _

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Oncotarget. 2014; 5:5845-5847. https://doi.org/10.18632/oncotarget.2286

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Delphine Gitenay1,2,3,4, Hélène Lallet-Daher1,2,3,4 and David Bernard1,2,3,4

1 Inserm U1052, Centre de Recherche en Cancérologie de Lyon, Lyon, France

2 CNRS UMR5286, Lyon, France

3 Centre Léon Bérard, Lyon, France

4 Université de Lyon, Lyon, France


David Bernard, email:

Keywords: caspase-2, senescence, cancer

Received: June 10, 2014 Accepted: July 31, 2014 Published: July 31, 2014


Cellular senescence is activated by numerous cellular insults, in particular those driving cancer formation, resulting in stable proliferation arrest and acquisition of specific features. By self-opposing to oncogenic stimulation, senescence is considered as a failsafe program, allowing, when functional, to inhibit cancers occurrence. Compelling evidences suggest a tumor suppressive activity of caspase-2, eventually independently of its effect on cell death. The original results described here demonstrate that this tumor suppressive activity of caspase-2 is mediated, at least in part, by its pro-senescing activity. Indeed, we have demonstrated in vitro and in vivo that loss of function of caspase-2 allows to escape oncogenic stress induced senescence. These results are discussed in the context of known tumor suppressive activity of caspase-2.

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