Caspase-2 regulates oncogene-induced senescence

Delphine Gitenay (1, 2, 3, 4) , Helene Lallet-Daher (1, 2, 3, 4) , David Bernard (1, 2, 3, 4)

1 UNICANCER/CRCL - Centre de Recherche en Cancérologie de Lyon
2 Laboratoire de Microbiologie
3 Centre Léon Bérard [Lyon]
4 Université de Lyon

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.

Mots clés: caspase-2; senescence; cancer

Domaines: Sciences du Vivant [q-bio]

Delphine Gitenay, Helene Lallet-Daher, David Bernard. Caspase-2 regulates oncogene-induced senescence. Oncotarget, 2014, 5 (14), pp.5845-5847. ⟨10.18632/oncotarget.2286⟩. ⟨hal-03108912⟩