Analysis for acetylation status of microtubules in epithelial mesenchymal transition induced by HGF/MET stimulation

本研究旨在探讨HDAC6在肝细胞癌（HCC）侵袭转移活动中的意义。我们还研究了HGF/MET系统对上皮间质转化的影响。与原代培养的肝细胞相比，HDAC6在所有HCC细胞系中的表达都更高。敲低HDAC6可显著下调所有HCC细胞系的迁移和侵袭活性（P<0.05）。70例原发性hcc中有14例（20%）HDAC6蛋白过表达高于相应的正常肝细胞，且与临床分期高、肿瘤数量多、血管侵犯及肝内转移相关（P<0.05）。HDAC6的下调抑制ERK1/2向核素的转运。这些结果表明HDAC6蛋白的过表达参与了HCC细胞的EMT。

The aim of this study was to investigate the significance of HDAC6 in the invasion and metastasis activities of hepatocellular carcinoma (HCC). And we also examined the effect on epithelial mesenchymal trsnsition induced by HGF/MET system. HDAC6 expression was greater in all of the HCC cell lines compared to the primary cultures of hepatocytes. Knockdown of HDAC6 markedly downregulated the migration and invasion activities of all HCC cell lines (P<0.05). Overexpression of HDAC6 protein to a level higher than that in the corresponding normal hepatocytes was observed in 14 (20%) of the 70 primary HCCs, and was significantly correlated with high clinical stage, number of tumors, vascular invasion and intrahepatic metastasis (P<0.05). Downregulation of HDAC6 inhibited ERK1/2 tranlocation to the nuclesu. These results suggest that overexpression of the HDAC6 protein is involved in EMT of HCC cells.