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

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 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