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

本研究旨在探讨HDAC 6在肝细胞癌（HCC）侵袭转移中的意义。并观察了HGF/MET系统对上皮间质转化的影响。HDAC 6表达在所有的HCC细胞系相比，肝细胞的原代培养物。HDAC 6基因的敲除可显著下调肝癌细胞的迁移和侵袭能力（P<0.05）。HDAC 6蛋白在70例原发性肝癌中有14例（20%）表达高于正常肝细胞，且与临床分期、肿瘤数目、血管浸润和肝内转移密切相关（P<0.05）。HDAC 6下调可抑制ERK 1/2向细胞核的转位。这些结果表明HDAC 6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.