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Title: Molecular mechanisms of euplotin C-induced apoptosis: involvement of mitochondrial dysfunction, oxidative stress and proteases
Authors: Cervia, Davide
Garcia-Gil, Mercedes
Simonetti, Elisa
Di Giuseppe, Graziano
Guella, Graziano
Bagnoli, Paola
Dini, Fernando
Keywords: Tumour cells;Cell death;Bax/Bcl-2;Δψm;ROS;Calpains
Issue Date: 2007
Publisher: Springer Verlag
Source: Cervia, D. et al. 2007. Molecular mechanisms of euplotin C-induced apoptosis: Involvement of mitochondrial dysfunction, oxidative stress and proteases. "Apoptosis" 12(8): 1349-1363
The metabolite euplotin C (EC), isolated from the marine ciliate Euplotes crassus, is a powerful cytotoxic and pro-apoptotic agent in tumour cell lines. For instance, EC induces the rapid depletion of ryanodine Ca2+ stores, the release of cytochrome c from the mitochondria, and the activation of caspase-3, leading to apoptosis. The purpose of this study was to gain further insight into the mechanisms of EC-induced apoptosis in rat pheochromocytoma PC12 cells. We found that EC increases Bax/Bcl-2 ratio and that Bax is responsible of the EC-induced dissipation of the mitochondrial membrane potential (Δψm). In addition, EC induces the generation of reactive oxygene species (ROS) without involvement of p53. The inhibition of ROS generation prevents, at least in part, the pro-apoptotic effects of EC as well as the effects of EC on Bax, Δψm and intracellular free Ca2+, indicating a cross-talk between different pathways. However, definition of the effector cascade turns out to be more complex than expected and caspase-independent mechanisms, acting in parallel with caspases, should also be considered. Among them, EC increases the expression/activity of calpains downstream of ROS generation, although calpains seem to exert protective effects.
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ISSN: 1360-8185
DOI: 10.1007/s10495-007-0075-7
Appears in Collections:DISA - Archivio della produzione scientifica

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