阿霉素对人乳腺癌细胞凋亡和增殖的影响  被引量:4

Effect of Adriamycin on Cell Apoptosis and Proliferation in Human Breast Cancer

在线阅读下载全文

作  者:王文武[1] 欧阳学农[1] 姜浩[2] 

机构地区:[1]南京军区福州总医院,福建福州350025 [2]南华大学附属第一医院,湖南衡阳421001

出  处:《中国肿瘤》2005年第3期189-191,共3页China Cancer

基  金:湖南省卫生厅课题(2001-Y58)

摘  要:[目的]检测阿霉素(ADR)对体外人乳腺癌化疗敏感细胞(MCF-7/S)凋亡和增殖的影响,并探讨其可能的作用机理。[方法]应用MTT比色法检测ADR对体外培养的MCF-7/S细胞增殖抑制作用,应用流式细胞术检测ADR诱导乳腺癌细胞凋亡,采用免疫细胞化学法检测ADR作用前后去磷酸化Rb蛋白和增殖细胞核抗原(PCNA)的表达。[结果]ADR抑制MCF-7/S细胞增殖,呈剂量依赖性;ADR组MCF-7/S细胞的凋亡率、磷酸化Rb蛋白的表达量与对照组相比明显增高(P<0.01);PCNA阳性表达率与对照组的相比明显降低(P<0.01)。在ADR组,MCF-7/S细胞的凋亡率(AR)与去磷酸化Rb蛋白的表达量呈正相关,与增殖细胞核抗原的阳性表达率呈负相关。[结论]ADR诱导MCF-7/S细胞凋亡并抑制MCF-7/S细胞增殖可能与其上调去磷酸化Rb蛋白和下调细胞内增殖细胞核抗原表达水平有关。To investigate the effects of adriamycin(ADR)on the apoptosis and proliferation of human breast cancer cells(MCF-7/S)cultured in vitro and to discuss the possible mechanism.MTT colorimetric assay and flow cytometry(FCM)were applied to examine the growth inhibition and apoptosis respectively.The expressive levels of dephosphorylated Rb protein and proliferating cell nuclear antigen(PCNA)were detected with immunocytochemistry in MCF-7/S cells.ADR inhibited proliferation of MCF-7/S cells in a dose-dependent manner.Tumor cell apoptotic rate (AR) and the expressive level of dephosphorylated Rb protein in ADR group were significantly higher than those in control group(P<0.01).PCNA positive expression rate in ADR group was significantly lower than that in control group(P<0.01).There was significant positive correlation between AR and the expressive level of dephosphorylated Rb protein in ADR group,but there was significant negative correlation between AR and PCNA.[Conclusions]ADR induces apoptosis and inhibits the growth proliferation in MCF-7/S cell,which is possibly related to the expression of ascending dephosphorylated Rb protein and descending PCNA.

关 键 词:乳腺肿瘤 细胞凋亡 阿霉素 去磷酸化RB蛋白 增殖细胞核抗原 

分 类 号:R737.9[医药卫生—肿瘤]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象