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• W2158933301 abstract "Nuclear factor kappaB (NF-kappaB) has been implicated in inducible chemoresistance against anthracyclines. In an effort to improve the cytotoxicity of anthracyclines while reducing their cardiotoxic effects, we have developed a novel class of extranuclear-localizing 14-O-acylanthracyclines that bind to the phorbol ester/diacylglycerol-binding C1b domain of conventional and novel protein kinase C (PKC) isoforms, thereby promoting an apoptotic response. Because PKCs have been shown to be involved in NF-kappaB activation, in this report, we determined the mechanism of NF-kappaB activation by N-benzyladriamycin-14-valerate (AD 198) and N-benzyladriamycin-14-pivalate (AD 445), two novel 14-O-acylanthracylines. We show that the induction of NF-kappaB activity in response to drug treatment relies on the activation of PKC-delta and NF-kappaB-activating kinase (NAK), independent of ataxia telengectasia mutated and p53 activities. In turn, NAK activates the IKK complex through phosphorylation of the IKK-2 subunit. We find that neither NF-kappaB activation nor ectopic expression of Bcl-X(L) confers protection from AD 198-induced cell killing. Overall, our data indicate that activation of novel PKC isoforms by cytoplasmic-targeted 14-O-acylanthracyclines promotes an apoptotic response independent of DNA damage, which is unimpeded by inducible activation of NF-kappaB." @default.
• W2158933301 created "2016-06-24" @default.
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• W2158933301 date "2004-03-25" @default.
• W2158933301 modified "2023-09-23" @default.
• W2158933301 title "Circumvention of Nuclear Factor κB-Induced Chemoresistance by Cytoplasmic-Targeted Anthracyclines" @default.
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• W2158933301 doi "https://doi.org/10.1124/mol.65.4.1038" @default.
• W2158933301 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15044634" @default.
• W2158933301 hasPublicationYear "2004" @default.
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