原肌球蛋白、丙酮酸激酶在急性早幼粒细胞白血病耐药细胞中表达上调  被引量:5

The up-regulation of tropomyosin and pyruvate kinase in retinoicacid resistent cells of APL

在线阅读下载全文

作  者:孙明莉[1] 李薇[2] 张一琼[2] 樊红琼[2] 王冠军[2] 

机构地区:[1]吉林大学第一医院急救医学科,吉林长春130021 [2]吉林大学第一医院血液肿瘤科,吉林长春130021

出  处:《中国实验诊断学》2007年第3期388-390,共3页Chinese Journal of Laboratory Diagnosis

摘  要:目的应用蛋白质组学方法筛选人急性早幼粒细胞白血病(APL)维甲酸敏感细胞株(NB4细胞株)和维甲酸耐药细胞株(NB4-R1细胞株)的耐药相关蛋白。方法利用双向凝胶电泳技术检测,比较NB4和NB4-R1细胞株的总蛋白,建立二维凝胶电泳(two-dimensional gel electrophoresis,2-DE)图谱。从多个差异蛋白质点中选择出2个在NB4-R1细胞株中表达明显上调的蛋白质点进行MALDI-TOF-MS生物质谱分析,并用Mascot软件在SwissProt和NCBInr数据库中进行同源比较和分析鉴定。结果确定表达明显上调的两个蛋白质分别为原肌球蛋白(tropomyosin,TM)和丙酮酸激酶(Pyruvate kinase,PK)。结论本研究表明维甲酸耐药细胞中原肌球蛋白和丙酮酸激酶表达上调,提示它们在肿瘤耐药中有重要作用。Objective To sift associated proteins of drug fast in human's acute promyelocyfic leukemia (APL) retinoicacid sensitive cell strain (NB4 cell strain) and refinoicacid resistent cell strain (NB4-R1 cell strain) by means of proteomic methods,so as to provide experimental foundation and theoretical basis of retinoicacid' s drug fast reversion. Methods The total proteins were compared in NB4 and NB4-R1 cell strains by two-dimensional polyacrylamide gel dectrophoresis detection and two-dimensional polyacrylamide gel electrophoresis atlas was established.2 significantly upregulated protein spots in NIM-R1 cell strain selected from several differentia protein spots were analyzed with biologic mass spectrometry technique MALDI-TOF-MS, and homologously compared and identiiied in SwissProt and NCBInr databases with Mascot software. Results The two proteins significantly upregulated were ascertained to be Tm(Tropomyosin) and PK(Pymvate kinase). Conclusion The research shows that Tm and PK are significantly upregulated in rctinoicacid resistent cells, which infers that Tm and PK play an important role in drug fast of neoplasm.

关 键 词:急性早幼粒细胞白血病 蛋白质组学 原肌球蛋白 丙酮酸激酶 

分 类 号:R733.71[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