Linked Life Data

9596684

Source:http://linkedlifedata.com/resource/pubmed/id/9596684

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pubmed-article:9596684pubmed:abstractTextThymidylate synthase (TS) inhibition causes cell death, and this enzyme is the target for the important chemotherapy regime 5-fluorouracil/leucovorin. GW1843 (1843U89) is a potent and specific folate analog TS inhibitor in clinical development. Because of the importance of TS as a chemotherapy target, we are studying the mechanism of TS inhibition-induced cell death by GW1843. Ceramide is a regulatory lipid generated by the action of sphingomyelinase and is believed to signal apoptosis. The role of the ceramide in apoptotic signaling was studied in Molt-4 human T-cell leukemia cells undergoing cell death after treatment with GW1843. In response to GW1843, Molt-4 cells undergo apoptosis with both acidic pH, Mg2+-independent sphingomyelinase (ASMase) and neutral pH, Mg2+-dependent sphingomyelinase (NSMase) activities elevated as early steps in the initiation of apoptosis before Molt-4 commitment to death. These activities lead to ceramide production with kinetics consistent with a role as an effector molecule signaling the initiation of apoptosis in Molt-4 cells. These changes were found to be independent of caspase 3-like (CPP32/apopain) activity and DNA degradation, but were not separable from membrane blebbing or cell lysis in this cell line. In this report, kinetic evidence is provided for a role of ceramide in initiating GW1843-induced cell death of Molt-4 T-cell leukemia cells.lld:pubmed
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pubmed-article:9596684pubmed:authorpubmed-author:SmithG KGKlld:pubmed
pubmed-article:9596684pubmed:authorpubmed-author:StrumJ CJClld:pubmed
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pubmed-article:9596684pubmed:dateRevised2007-11-15lld:pubmed
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pubmed-article:9596684pubmed:articleTitleIncreases in neutral, Mg2+-dependent and acidic, Mg2+-independent sphingomyelinase activities precede commitment to apoptosis and are not a consequence of caspase 3-like activity in Molt-4 cells in response to thymidylate synthase inhibition by GW1843.lld:pubmed
pubmed-article:9596684pubmed:affiliationInternational Science Development Group, Glaxo Wellcome Inc, Research Triangle Park, NC 27709, USA.lld:pubmed
pubmed-article:9596684pubmed:publicationTypeJournal Articlelld:pubmed