期刊文献+

乳腺癌耐药细胞中mdr-1与mrp基因的表达及As_2O_3对其表达的影响

The Expression of mdr-1 and mrp Genes in the Human Breast Cancer Cells, and the Effects of Arscenic Trioxide on the Gene Expression
下载PDF
导出
摘要 目的:探讨人乳腺癌阿霉素(ADM)耐药细胞系MCF-7/ADM的mdr-1基因和mrp基因表达,观察三氧化二砷(As_2O_3)对上述基因表达的影响。方法:采用MTT法检测As_2O_3的细胞毒性及非细胞毒性剂量,应用RT-PCR检测mdr-1基因和mrp基因的转录表达。结果:As_2O_3的非细胞毒性剂量为0.2μmol/L,低毒计量为0.8μmol/L。mdr-1基因和mrp基因在MCF-7/ADM细胞中均呈过表达,而且mdr-1的基因表达强于mrp基因,在MCF-7/S细胞中未见表达。As_2O_3可下调上述基因的表达,而且As_2O_3低毒剂量的下调作用强于无毒剂量。结论:人乳腺癌MCF-7/ADM细胞获得阿霉素抗药性,与mdr-1基因和mrp基因过表达有关,As_2O_3可通过多种机制部分逆转MCF-7/ADM细胞的耐药性。 Objective: To investigate the expression of mdr-1 and mrp genes and observe the effects of arsenic trioxide (As_2O_3) on the gene expression. Methods: The doze of cytotoxicity and non-cytotoxicity of As_2O_3 was examined through MTT assay. The expressions of mdr-1 and mrp genes were studied by RT-PCR method. Results: The non-cytotoxic dose of As_2O_3 was 0. 2μmol/L and the low cytotoxic dose was 0. 8μmol/L to MCF-7/ADM cell line(P<0. 05). Expression of mdr-1 and mrp genes was positive in MCF-7/ADM cells, and the expression of mdr-1 was stronger than the mrp gene, then the expression of mdr-1 and mrp genes was negative in the MCF-7/S cells; Arsenic trioxide could down-regulate the expression of mdr-1 and mrp genes in MCF-7/ADM and the lowcytotoxic dose of As_2O_3 had more strong effect than the non-cytotoxic dose of As_2O_3. Conclusions: The strong expressions of mdr-1 and mrp genes were responsible for the in- duced resistance of MCF-7/ADM cells to ADM; Arsenic trioxide reverses partly the multidrug resistance of the MCF-7/ ADM cells with more kinds of biologic mechanisms.
出处 《中国肿瘤生物治疗杂志》 CAS CSCD 2003年第4期285-288,共4页 Chinese Journal of Cancer Biotherapy
基金 辽宁省教委重点资助项目(7907111010)
关键词 MDR-1基因 MRP基因 多药耐药 AS2O3 乳腺肿瘤 mdr-1 gene mrp gene MDR As_2O_3 breast neoplasm RT-PCR
  • 相关文献

参考文献4

二级参考文献27

  • 1刘岳彪,吴德政.阿霉素耐药与谷胱甘肽-S-转移酶[J].肿瘤,1994,14(2):117-119. 被引量:5
  • 2[1]Chung HC, Rha SY, Kim JH, et al. P-glycoprotein:the intermediate end point of drug response to induction chemotherapy in locally advanced breast cancer[J].Breast Cancer Res Treat,1997,42:65.
  • 3[2]Izquierdo MA, Scheffer GL, Flens MJ, et al. Relationship of LRP-human major vault protein to in vitro and clinical resistance to anticancer drugs[J].Cytotechnology,1996,19:191.
  • 4[3]Bellamy CO, Harrison DJ. Evaluation of glutathione S-transferase Pi in non-invasive ductal carcinoma of breast[J].Br J Cancer,1994,69:183.
  • 5[4]Hosking LK, Whelan RD, Shellard SA, et al. Multiple mechanisms of resistance in a series of human testicular teratomacell lines selected for increasing resistance to etoposide[J].Int J Cancer,1994,57:259.
  • 6[5]Vanhoefer U, Yin MB, Harstrick A, et al. Carbamoylation of glutathione reductase by N,N-bis(2-chloroethyl)N-nitrosourea associated with inhibition of multidrug resistance protein(MRP) function[J].Biochenm Pharmacol,1997,53:801.
  • 7[6]Szakas G, Jakab K, Antal F, et al. Diagnostics of multidrug resistance in cancer[J].Pathol Oncol Res,1998,4:251.
  • 8Wallner J, Depisch D, Hopfner M, et al. MDR-1 gene expression and prognostic facter in primary breast carcinomas. Eur J Cancer,1991,27:1352.
  • 9Hennequin E, Delvincourt C, Pourny C, et al. Expression of mdr-I gene in human breast primary tumors and metastases.Breast Cancer Res Treat, 1999,26,267.
  • 10Schneider E, Horton JK, Yang CH, et al. Multidrug resistance associated protein gene overexpression and reduced drug sensitivity of topoisomerase in a human breast carcinoma MCF7 cell line selected for etoposide resistance. Cancer Res,1994,54,152.

共引文献52

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部