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作 者:夏江宝[1,2] 邢晓华[2] 王英超[2] 沈佐君[3]
机构地区:[1]蚌埠医学院医学检验系,安徽蚌埠233030 [2]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 [3]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
出 处:《福州大学学报(自然科学版)》2016年第2期282-288,共7页Journal of Fuzhou University(Natural Science Edition)
基 金:福建省自然科学基金资助项目(2015J05174);福建省卫生计生委青年科研课题资助项目(2015-1-94);福州市科技强院建设项目(编号:2014-S-139-3);福建医科大学孟超肝胆医院科研资助项目(QDZJ-2014-005);福建中医药大学校管科研课题资助项目(XB2014096)
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.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 Hep G2 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 /2and 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.
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
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