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Cisplatin Cytotoxicity: DNA and Plasma Membrane Targets

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Most current anticancer therapies induce tumor cell death through apoptosis where its specific involved pathways are poorly understood. For example, for many DNA-damaging agents, the specific biochemical lesions (DNA adducts) are associated with the induction of apoptosis via the mitochondria death pathway. However, several of these DNA-damaging agents like cisplatin induce apoptosis through plasma membrane disruption, triggering the Fas death receptor pathway. In this review, we focus on the role of early plasma membrane events in cisplatin-induced apoptosis. Special attention is given to changes in plasma membrane fluidity, inhibition of NHE1 exchanger, activation of acid sphingomyelinase and their consequences on the Fas death pathway in response to cisplatin.

Keywords: DNA adducts; Fas death receptor; Na+/H+ exchanger 1 (NHE1); acid sphingomyelinase; membrane fluidity; membrane lipid rafts

Document Type: Research Article


Affiliations: Inserm, UMR620, IFR 140 GFAS, Rennes, F35043; EA SeRAIC, University of Rennes 1, Rennes, F35043, France.

Publication date: November 1, 2008

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  • Current Medicinal Chemistry covers all the latest and outstanding developments in medicinal chemistry and rational drug design. Each issue contains a series of timely in-depth reviews written by leaders in the field covering a range of the current topics in medicinal chemistry. Current Medicinal Chemistry is an essential journal for every medicinal chemist who wishes to be kept informed and up-to-date with the latest and most important developments.

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