Publication: Different patterns of apoptosis in response
to cisplatin in B50 neuroblastoma rat cells
Authors
Santin, G. ; Piccolini, V.M. ; Veneroni, P. ; Barni, Sergio ; Bernocchi, G. ; Bottone, M.G.
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Publisher
F. Hernández y Juan F. Madrid. Murcia: Universidad de Murcia, Departamento de Biología Celular e Histología
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Cisplatin (cisPt) is a chemotherapeutic drug
used for several human malignancies. CisPt cytotoxicity
is primarily mediated by its ability to cause DNA
damage and subsequent apoptotic cell death. DNA is the
primary target of cisPt; however, recent data have shown
that cisPt may have important direct interactions with
mitochondria, which can induce apoptosis and may
account for a significant part of the clinical activity
associated with this drug. We have previously
demonstrated that in the rat neuronal cell line B50, at 20
h-treatment with cisPt activates apoptosis through an
intrinsic pathway involving an alteration of
mitochondrial membrane permeability and the release of
cytochrome c. The present study investigates different
death pathways induced in the same cell line by a
prolonged treatment with 40 µM cisPt for 48 h. To
address this issue, we focused on caspases-8 and -12,
and on the mitochondrial apoptosis inducing factor
(AIF), which translocates to the nucleus and induces cell
death via caspase-independent pathway. We found that
cisPt activates different forms of cell death, i.e. the
receptor-mediated apoptotic extrinsic pathway and a
death process mediated by endoplasmic reticulum stress.
Moreover, we demonstrated that AIF-mediated death
occurs, being characterized by the translocation of AIF
from mitochondria to the nucleus. On the whole, we
provided evidence that prolonged cisPt treatment is able
to activate both caspase-dependent and caspaseindependent
apoptotic pathways in B50 rat neuronal
cells.
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