摘要
目的观察耐药乳腺癌细胞c-myc表达及其反义寡核苷酸对耐药的逆转效应,探讨c-myc在耐药调控中的作用。方法运用流式细胞仪检测乳腺癌耐药细胞MCF-7/Adr和其药敏亲本系MCF-7的c-myc表达水平。MTT法测定阿霉素作用于上述细胞的药物半数抑制浓度(IC50)。结果MCF-7/Adr耐药细胞c-myc的表达率为70.48%,其亲本药敏细胞系MCF-7c-myc表达率仅46.02%,前者显著高于后者(P<0.05)。阿霉素单独作用于MCF-7/Adr,IC50值为(22.00±1.92)μmol/L,但与4μmol/Lc-myc反义寡核苷酸共孵育后,阿霉素的IC50值则显著下降为(9.60±1.04)μmol/L。结论与其亲本药敏细胞相比较,MCF-7/Adr的c-myc表达显著上调,抑制c-myc的过表达可部分逆转MCF-7/Adr的阿霉素抵抗,提示c-myc参与肿瘤耐药的发生。
Objective To investigatetheexpressionof c-my c indrug-resistantMCF-7/Adrhumanbreastcancercellsandthe counteractiveeffectof c-my c antisenseoligonucleotideon theirdrug-resistance.Methods Flowcytometrywas performedto examinec-my c expressionin multi-drugresistantMCF-7/AdrcelllineanditsparentalcelllineMCF-7.The IC 50 valueof doxorubicinwasevaluatedby MTTassay.Results MCF-7/Adrcelllinewasshownto havea significantlyhigherexpression rateof c-my c thanitsparentcelllineMCF-7(70.48%vs46.02%).TheIC 50 valueof doxorubicinwas(22.00±1.92)μmol/Lin MCF-7/Adrcells,whichwassignificantlydecreasedto(9.60±1.04)μmol/L(P<0.05)aftercoincubationwith4μmol/Lc-my c antisenseoligonecleotide.Conclusion c-my c expressionis up-regulatedinMCF-7/Adrcellsas comparedwiththeirparentcell lineMCF-7.Inhibitionof c-my c expressionmaypartiallyreversetheresistanceof MCF-7/Adragainstdoxorubicin,suggesting thatc-myc maybe involvedinthemechanismof drug-resistanceof tumorcells.
出处
《第一军医大学学报》
CSCD
北大核心
2002年第2期124-126,共3页
Journal of First Military Medical University
基金
国家自然科学基金(30100045)
关键词
乳腺肿瘤
MYC基因
反义寡核苷酸类
多药抗药性
阿霉素
breastneoplasms
gene,myc
oligonucleotides,antisense
drugresistance,multiple
doxorubicin
