期刊文献+

蛋白酶体抑制剂MG132对宫颈癌SiHa细胞中p53蛋白泛素化降解的影响 被引量:1

Effect of proteasome inhibitor MG132 on ubiquitination degradation of p53 protein in SiHa cells
原文传递
导出
摘要 目的探讨蛋白酶体抑制剂MG132对人宫颈癌SiHa细胞中p53蛋白泛素化降解的影响。方法采用MTT法筛选的不同浓度蛋白酶体抑制剂MG132处理SiHa细胞,通过Western blot法测定细胞内p53蛋白相对含量(以GAPDH为内参),同时设未处理组(未加入MG132)。结果20μmol/L为不影响SiHa细胞活性的MG132最大浓度,因此选用低于该浓度的1、3和5μmol/L MG132处理SiHa细胞。经1、3和5μmol/L MG132处理的SiHa细胞中p53蛋白相对表达量分别为1.210±0.252、1.057±0.130和1.475±0.210,均明显高于未处理组(0.034±0.026),差异均有统计学意义(P<0.001),且MG132对p53降解的抑制作用呈剂量依赖性(P<0.01)。结论蛋白酶体抑制剂MG132可抑制SiHa细胞内p53蛋白泛素化降解,且呈剂量依赖性。 Objective To investigate the effect of proteasome inhibitor MG132 on the ubiquitination degradation of p53 protein i n human cervical cancer SiHa cells.Methods SiHa cells were treated with different concentrations of proteasome inhibitor MG132 screened by MTT assay,and determined for the relative expression levels of p53 protein by Western blot,using GAPDH as an internal reference,and the cells untreated as control.Results The maximum MG132 concentration without influence on SiHa cell activity was 20μmol/L,thus the cells were treated with MG132 at the concentrations of 1,3 and 5μmol/L(less than 20μmol/L).The relative expression levels of p53 in SiHa cells treated with 1,3 and 5μmol/L of MG132 were 1.210±0.252,1.057±0.130 and 1.475±0.210 respectively,which were significantly higher than that in the untreated cells(0.034±0.026)(P<0.001).The inhibitory effect of MG132 on p53 degradation was dose-dependent(P<0.01).Conclusion The proteasome inhibitor MG132 inhibits the ubiquitination degradation of p53 in SiHa cells in a dose-dependent pattern.
作者 王樱槥 郭宇微 林迎伟 赵春艳 WANG Ying-hui;GUO Yu-wei;LIN Ying-wei;ZHAO Chun-yan(Department of Clinical Biochemistry,College of Laboratory Medicine,Dalian Medical University,Dalian 116044,Liaoning Province,China)
出处 《中国生物制品学杂志》 CAS CSCD 2020年第5期498-500,506,共4页 Chinese Journal of Biologicals
基金 辽宁省自然科学基金(20180530100)。
关键词 MG132 宫颈癌 SIHA细胞 泛素化蛋白酶体途径 p53 MG132 Cervical cancer SiHa cells Ubiquitin proteasome pathway p53
  • 相关文献

参考文献2

二级参考文献9

共引文献311

同被引文献16

引证文献1

二级引证文献1

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