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维普资讯
现代肿瘤医学 2008年 5月 第 l6卷第 5期 ·7l3·
rmhTRAIL诱导耐阿霉素细胞株 K562/A02凋亡及作用机制的实验研究
王雅茹 ,王福旭 ,温树鹏 ,杜行严 ,杨渤彦 ,张学军 ,杨世方
Themechanism oftheapoptosisoftheleukemiacelllineK562resistanttoAdriamycin
K562/A02inducedbyrmhTRAIL
WANGYa—ru,WANGFu—xu,WENShu—peng,DUXing—yan,YANGBo—yan,ZHANGXue—j.n,YANGShi
— · fang
DepartmentofHematology,TheThird日 豇 ,Baoding071000,China.
【Abstract】 Objective:Toinvestigatetheapoptosismechanismofmulti—drugresistantcelllineK562/A02(mdr
一 1)inducedbyrmhTRAIL.Methods:K562(mdr一1一)wfiscontrolled,morphologywgsobservedbeforenad
aftertreatmentofrmhTRALL;Flow c~ometerwlit8usedtoanaiy~ hteapoptoticpeakofvfriousconcenrtationsof 1Tn-
hTRAIL;MTrtoassayhtegrowthinhibitoryeffectofrmhTRAIL;ThedifferentmRNA expressionlevelsofDR4,
DR5,DcR1,DcR2ofK562na dK562/A02cellswere examinedbysemi—qunatitativereversetrna scriptionpolymer-
88echainreactionRT—PCR.Results:Th eapoptosisofK562,K562/A02cellsinducedbyrmhTRAILwlit8observed
atacytomorphologynagle,withtypicalcytmorphologlcaichnages;TheapoptosisratioofK562/A02groupsurpassed
K562(P0.05);TheinhibitionofK562/A02cellssuprassedtheK562(P0.05);K562/A02cellsexpressed
DR4mRNA na dDR5 mRNA higherhtna K562,hteexpressionofDcR1onK562/A02cellswas lowerhtna K562,
DcR2mRNA didnotexpressintwokindofcells.Conclusion:rmhTRAILCallinduceK562na dK562/A02cells印-
optosis;Th eefficacyofrmhTRAILtoinduceapo ptosisnadihnibitproliferationinK562/A02celllineismorepre-
dominnatthna hteirparentalcelllineinhtestudy;Th ehishexpressionofdeaht receptors nadhtelow expressionof
decoyreceptors couldbeoneofhtereasonshtatK562/A02cellswere more sensitivehtna K562.
【Keywords】tumornecrosisfacotr—relatedapoptosis—inducinglignad;mdr一1;K562;K562/A02;apoptosis;
r
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