文章摘要
引用本文:夏江宝,邢晓华,王英超,沈佐君.无标记定量蛋白质组学分析AMACR过表达对肝癌细胞生物学行为的影响[J].福州大学学报(自然科学版),2016,44(2):282~288
无标记定量蛋白质组学分析AMACR过表达对肝癌细胞生物学行为的影响
Label-free quantitative proteomic analysis of the effect of AMACR overexpression on biological behaviors of hepatocellular carcinoma cells
  
DOI:10.7631/issn.1000-2243.2016.02.0282
中文关键词: 肝细胞癌  α-甲酰基辅酶A消旋酶  细胞增殖  无标记定量蛋白质组学
英文关键词: hepatocellular carcinoma  AMACR  cell proliferation  label-free quantitative proteomics
基金项目:
作者单位
夏江宝 蚌埠医学院医学检验系安徽 蚌埠 233030 福建省联合创新重点实验室福建医科大学孟超肝胆医院福建 福州 350025 
邢晓华 福建省联合创新重点实验室福建医科大学孟超肝胆医院福建 福州 350025 
王英超 福建省联合创新重点实验室福建医科大学孟超肝胆医院福建 福州 350025 
沈佐君 安徽医科大学附属省立医院安徽省临床检验中心安徽 合肥 230001 
摘要点击次数: 345
全文下载次数: 250
中文摘要:
      研究α-甲酰基辅酶A消旋酶(AMACR)过表达对肝癌细胞生物学行为的影响及其分子机制. 首先建立AMACR稳定过表达细胞株,然后提取AMACR过表达细胞株的全蛋白,进行无标记定量蛋白质组学研究,最后对鉴定结果进行生物信息学分析和结果验证,共筛选出138种差异表达蛋白. 这些差异表达蛋白主要参与代谢加工、细胞加工等,证明AMACR的过表达对于肝癌细胞的生物学行为影响巨大. IPA分析发现,这些差异表达蛋白主要参与了ERK1/2信号通路和NF-κB信号通路. 以上结果说明,AMACR的过表达通过调节ERK1/2和NF-κB信号通路等手段改变肝癌细胞的生物学行为.
英文摘要:
      This study attempted to investigate the effect of AMACR overexpression on the biological behavior of HCC cells using label free quantitative proteomic approch. A stable cell line that overexpressed AMACR was produced by transducing engineered lentivirus containing AMACR complete sequence into HepG2 cells. Afterwards,the whole protein extracted from the AMACR-overexpressed cells and the normal cultured cells (control) were comparatively quantified by 2D LC-MS/MS. A total of 138 differentially expressed proteins were identified. These dysregulated proteins were mostly enriched for metabolic process and cellular process,which suggested a big change at biological behaviors occurred in the host cells due to AMACR overexpression. The signalings pathway analysis revealed that the dysregulated proteins in AMACR-overexpressed cells are more concentrated to the ERK1/2 and NF-κB signaling pathways. Thus,AMACR overexpression induced the alterations at biological behaviors of HCC cells majorly through modulating the ERK1/2 and NF-κB signalings.
查看全文   查看/发表评论  下载PDF阅读器
关闭