摘要
目的:研究MCF-7人乳腺癌细胞阿霉素敏感株(MCF-7细胞)和耐药株(MCF-7/ADR细胞)中雌激素受体(estrogenreceptor,ER)表达的变化与其对细胞生物学特性的影响。方法:应用Westernblot法检测MCF-7细胞和MCF-7/ADR细胞中雌激素受体表达,MTT法检测细胞增殖及细胞对雌激素(es-trogen,E2)和droloxifene(Dro)的敏感性,流式细胞仪检测细胞周期变化。结果:Westernblot证实在MCF-7细胞中ER为阳性,而在MCF-7/ADR细胞中ER为阴性。经MTT分析,与MCF-7相比,MCF-7/ADR细胞生长速度减慢,细胞多分布于G0/G1期。E2在1×10-12mol/L的浓度时开始促进MCF-7细胞的生长,到达1×10-9mol/L时促生长作用进入平台期;而任何浓度的E2对MCF-7/ADR细胞均无促生长作用。Dro的浓度达到10μmol/L的时候,开始出现对MCF-7细胞生长的抑制,抑制程度随浓度的增加而逐渐增强;Dro浓度小于20μmol/L时,对MCF-7/ADR细胞生长无明显作用,当浓度达到20μmol/L时对MCF-7/ADR细胞的生长出现明显抑制,且高于对MCF-7细胞的抑制。结论:MCF-7/ADR细胞雌激素受体表达缺失,生长速度减慢,同时细胞失去对雌激素的依赖性,并对一定浓度的内分泌治疗药物不敏感。
Objective:To study the alteration and significance of ER status in Adriamycin-sen-sitive and Adriamycin-resistant MCF-7human breast cancer cell lines.Methods:The status of ER of MCF-7/ADR and parental MCF-7cells was detected by Western blot.The growth and the sensitivity to Estrogen(E 2 )and droloxifene(Dro)of cells were investigated by MTT assay,and the distribution of cell cycle was detected by flow cytometric assay.Results:ER was positive in MCF-7cells,but negative in MCF-7/ADR cells.In comparison with MCF-7cells,MCF-7/ADR cells showed lower growth rate,and the cell cycle was arrested at G 0 /G 1 phase.E 2 at concentrations between1×10 -12 mol/L and1×10 -7 mol/L significantly stimulated the growth of MCF-7,but did not stimulate the growth of MCF - 7/ADR.Dro at concentrations between10μmol/L and20μmol/L significantly inhibited the growth of MCF-7,and the inhibition was dose-dependent.Dro at concentrations below20μmol/L did not inhibit the growth of MCF-7/ADR,Dro inhibited the growth of MCF-7/ADR only at the concentration of20μmol/L,and the inhibition was more effective than that of MCF-7.Conclusion:ER is lost and the growth rate de-creases in MCF-7/ADR cells,at the same time MCF-7/ADR cells loses the dependence on estrogen and the sen sitivity to endocrine therapy.
出处
《山东大学学报（医学版）》
CAS
2003年第2期181-184,共4页
Journal of Shandong University:Health Sciences
关键词
乳腺肿瘤
耐药性
雌激素受体
内分泌治疗
Breast neoplasms
Drug resistance
Estrogen receptor
Endocrine therapy
