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dc.contributor.authorBazill, G W
dc.contributor.authorDexter, T Michael
dc.date.accessioned2010-08-17T13:30:19Z
dc.date.available2010-08-17T13:30:19Z
dc.date.issued1990-12-01
dc.identifier.citationRole of endocytosis in the action of ether lipids on WEHI-3B, HL60, and FDCP-mix A4 cells. 1990, 50 (23):7505-12 Cancer Res.en
dc.identifier.issn0008-5472
dc.identifier.pmid2253199
dc.identifier.urihttp://hdl.handle.net/10541/109765
dc.description.abstractWe investigated the effect of a number of platelet activating factor antagonists on cell killing by 1-O-octadecyl-2-O-methyl-sn-glycero-3-phosphoryl choline (ET-18-OCH3). Of six platelet activating factor antagonists tested, four were found to protect WEHI-3B leukemic cells against cell death induced by ET-18-OCH3. Certain other compounds, not platelet activating factor antagonists, had similar protective effects. The protective compounds were all lipophilic weak bases. We describe experiments that indicate that these compounds protect by inhibition of endocytic uptake of ET-18-OCH3. Sensitive cells showed rapid endocytic uptake, whereas in resistant cells, uptake was slow. Uptake of ET-18-OCH3 could be suppressed by inhibitors of endocytosis such as chloroquine, monensin, and vinblastine. We conclude that one of the principal determinants of sensitivity or resistance to ether lipids may be the rate at which cells take them up by endocytosis.
dc.language.isoenen
dc.subjectAnticancerous Agentsen
dc.subjectMyeloid Leukaemaien
dc.subject.meshAnimals
dc.subject.meshAntineoplastic Agents
dc.subject.meshAzepines
dc.subject.meshCell Survival
dc.subject.meshChloroquine
dc.subject.meshDiltiazem
dc.subject.meshDrug Synergism
dc.subject.meshEndocytosis
dc.subject.meshFurans
dc.subject.meshHumans
dc.subject.meshHydroxyzine
dc.subject.meshLeukemia, Myeloid
dc.subject.meshMice
dc.subject.meshNifedipine
dc.subject.meshPhospholipid Ethers
dc.subject.meshPlatelet Activating Factor
dc.subject.meshPyridines
dc.subject.meshQuinidine
dc.subject.meshQuinine
dc.subject.meshSodium Fluoride
dc.subject.meshThiazoles
dc.subject.meshTriazoles
dc.subject.meshVerapamil
dc.titleRole of endocytosis in the action of ether lipids on WEHI-3B, HL60, and FDCP-mix A4 cells.en
dc.typeArticleen
dc.contributor.departmentDepartment of Experimental Haematology, Paterson Institute for Cancer Research, Christie Hospital, Manchester, United Kingdom.en
dc.identifier.journalCancer Researchen
html.description.abstractWe investigated the effect of a number of platelet activating factor antagonists on cell killing by 1-O-octadecyl-2-O-methyl-sn-glycero-3-phosphoryl choline (ET-18-OCH3). Of six platelet activating factor antagonists tested, four were found to protect WEHI-3B leukemic cells against cell death induced by ET-18-OCH3. Certain other compounds, not platelet activating factor antagonists, had similar protective effects. The protective compounds were all lipophilic weak bases. We describe experiments that indicate that these compounds protect by inhibition of endocytic uptake of ET-18-OCH3. Sensitive cells showed rapid endocytic uptake, whereas in resistant cells, uptake was slow. Uptake of ET-18-OCH3 could be suppressed by inhibitors of endocytosis such as chloroquine, monensin, and vinblastine. We conclude that one of the principal determinants of sensitivity or resistance to ether lipids may be the rate at which cells take them up by endocytosis.


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