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Poly(ADPR)polymerase inhibition and apoptosis induction in cDDP-treated human carcinoma cell lines.

Abstract：

:Poly(ADPR)polymerases' (PARPs) inhibitors potentiate the cytotoxic effects of chemotherapeutic agents like alkylating compounds and TOPO I poisons, while their action in combination with cisplatin still needs investigation. In fact, one of the earliest responses to DNA single- or double-strand breaks is the synthesis of poly(ADP-ribose) (PAR) by PARPs; these enzymes are components of DNA repair machineries and substrates of caspases. Cisplatin (cDDP) yields intra- and inter-strand DNA cross-links and several proteins that recognise cDDP-induced DNA damage, such as p53, are also targets of poly(ADP-ribosyl)ation. We compared the effects of treatments with cDDP and the PARPs inhibitor PJ34 in p53 mutated carcinoma cell lines (HeLa, KB, HT29) that exhibited differential sensitivities to the drugs, in terms of cell growth inhibition and onset of apoptosis. In cDDP-resistant HT29 cells we determined: (i) PJ34 potentiation of cDDP-induced cell growth inhibition; (ii) an increment of PARP-1 automodification following cDDP treatment. In cDDP-sensitive HeLa cells, we found that the drug induced apoptotic cell death associated with caspase-dependent PARP-1 proteolysis.

journal_name

Biochem Pharmacol

journal_title

Biochemical pharmacology

authors

Gambi N,Tramontano F,Quesada P

doi

10.1016/j.bcp.2008.03.015

subject

Has Abstract

pub_date

2008-06-15 00:00:00

pages

2356-63

issue

12

eissn

0006-2952

issn

1873-2968

pii

S0006-2952(08)00197-4

journal_volume

75

pub_type

杂志文章

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