miR-155通过调节Ets-1逆转白血病细胞阿霉素耐药的研究
- 1、下载文档前请自行甄别文档内容的完整性,平台不提供额外的编辑、内容补充、找答案等附加服务。
- 2、"仅部分预览"的文档,不可在线预览部分如存在完整性等问题,可反馈申请退款(可完整预览的文档不适用该条件!)。
- 3、如文档侵犯您的权益,请联系客服反馈,我们会尽快为您处理(人工客服工作时间:9:00-18:30)。
miR-155通过调节Ets-1逆转白血病细胞阿霉素耐药的研究沙敏;叶军;郭婷;张立新;栾正云
【期刊名称】《临床肿瘤学杂志》
【年(卷),期】2015(000)012
【摘要】Objective To detect the expression of miR⁃155 and Ets⁃1 in leukemia cell line K562 and adriamycin resistance K562/A02 cell line, and explore the relationship between miR⁃155, Ets⁃1 and drug resistance in leukemia treatment. Methods miR⁃155 simulation oligonucleotide probes and miR⁃155 inhibitor oligonucleotide probes, Ets⁃1 expression plasmid and Ets⁃1 interference expression plasmid were transfected in K562 and
K562/A02 cells by Lipofectamine 2000. Real⁃time quantitative PCR was used to de⁃termine the expression of miR⁃155, Ets⁃1 and multidrug resistance( MDR1) . The protein levels of Ets⁃1 and MDR1 were analyzed by Western blotting. The viability of K562 and K562/A02 cells was evaluated by MTT assay. Results The expression levels of miR⁃155, Ets⁃1 and MDR1 were significantly increased in K562/A02 cells than those in K562 cells. Down⁃regulation of miR⁃155 could obviously increase the inhibition rate of adriamycin on K562/A02 cells and inhibit the expression of Ets⁃1 and MDR1, which could be reversed by overexpression of Ets⁃1. While,
up⁃regulation of miR⁃155 could significantly increase the inhibition rate of adriamycin on K562 cells and stimulate the expression of Ets⁃1 and MDR1, which could be reversed by Ets⁃1 siRNA. Conclusion miR⁃155 is involved in
the mechanism of drug resistance in leukemia by regulating Ets⁃1 expression, which may provide a potential novel target for overcoming drug⁃resistance.%目的通过检测人白血病细胞株K562及阿霉素耐药细胞株
K562/A02中miR⁃155和Ets⁃1表达,探讨miR⁃155、Ets⁃1表达与白血病化疗耐药的关系。
方法利用Lipofectamine 2000将含有miR⁃155模拟物和miR⁃155抑制物的寡核苷酸探针、Ets⁃1过表达质粒以及Ets⁃1干扰质粒转染K562及
K562/A02细胞,实时荧光定量PCR法检测miR⁃155、Ets⁃1及多药耐药基因( MDR1)的表达,Western blotting检测Ets⁃1和MDR1蛋白表达水平;转染后的K562及K562/A02细胞经阿霉素处理24 h,MTT法检测细胞存活率。
结果与K562细胞相比,K562/A02细胞中miR⁃155、Ets⁃1和MDR1表达水平显著升高( P<0�05)。
抑制miR⁃155表达能显著增强阿霉素对K562/A02细胞的抑制作用,并抑制Ets⁃1和MDR1表达,而MDR1表达抑制效应可被Ets⁃1过表达所逆转。
结论 miR⁃155通过调节Ets⁃1表达参与白血病耐药形成,
miR⁃155有可能成为逆转白血病耐药的作用靶点。
【总页数】5页(P1063-1067)
【作者】沙敏;叶军;郭婷;张立新;栾正云
【作者单位】225300 江苏泰州泰州市人民医院临床医学研究所;225300 江苏泰州泰州市人民医院临床医学研究所;225300 江苏泰州泰州市人民医院临床医学研究所;225300 江苏泰州泰州市人民医院临床医学研究所;225300 江苏泰州泰州市人民医院临床医学研究所
【正文语种】中文
【中图分类】R733.7
【相关文献】
1.苦参碱逆转人白血病K562/ADM细胞对阿霉素耐药性的研究 [J], 丁艳芳;谢霞;赵瑾瑶;杨佩满
2.阿霉素纳米粒对白血病耐药细胞株K562/DOX耐药逆转作用的研究 [J], 王华芳;胡豫;郑金娥;周薇;方峻
3.SiRNA逆转人红白血病细胞株(K562/ADM)阿霉素耐药性的实验研究 [J], 周冬梅;郑雄伟
4.阿霉素纳米粒对人白血病多药耐药细胞株HL-60/ADR多药耐药性的逆转作用[J], 王磊;柯红;任东明;王一羽
5.MDR1基因下调逆转人白血病阿霉素耐药细胞株K562/ADM的耐药性 [J], 魏玲;宋现让;孙菊杰;王兴武;宋宝;郑燕
因版权原因,仅展示原文概要,查看原文内容请购买。