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A recent study showed that both 5-fluorouracil (5FU)-stimulated apoptosisand Fas-mediated apoptosis in human endometrial adenocarcinoma cells are enhancedby targeted knockdown of endogenous death-associated protein kinase (DAPK) withDAPK small-interfering RNAs. Therefore, we investigated the DAPK survival signalsin three 5FU-resistant subclones. DAPK knockdown did not enhance 5FU-stimulatedor Fas-mediated apoptosis in any of the three 5FU-resistant subclones, but thesubclones acquired resistance to VP16-stimulated cell death that was DAPK-independent.Semi-quantitative flow cytometric analyses showed that there was no differentialexpression in nine cell surface antigens, including Fas, and six intracellularmolecules, including DAPK, that may regulate cell death or survival between theparent cells and 5FU-resistant cells. DAPK mRNA and protein were expressed inthe 5FU-resistant subclones at similar levels to the parent cells. These resultsindicate that acquisition of 5FU-resistance may be accompanied by impairment ofcommon apoptotic signals regulating both DAPK-dependent and DAPK-independent pathways.

Impaired death-associated protein kinase-mediated survival signals in 5-fluorouracil-resistant human endometrial adenocarcinoma cells