G-W Feng1, L-D Dong, W-J Shang, X-L Pang, J-F Li, L Liu, Y Wang. 1. Department of Renal Transplantation, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. shangwenjun0108@126.com.
Abstract
OBJECTIVES: Histone deacetylases (HDACs) plays important roles in the regulation of genes expression and contribute to the growth of cancer cells. The present study aimed to investigate the function of HDAC5 in human hepatocellular carcinoma (HCC). PATIENTS AND METHODS: The expression of HDAC5 in human hepatocellular carcinoma tissues and cells was detected. MTT assay was used to measure the proliferation of HCC cell lines. siRNA technology was employed to down-regulate the protein expression of HDAC5 and Six1. RESULTS: Western blot showed that the HDAC5 expression was increased in human HCC tissues. The mRNA and protein levels of HDAC5 were up-regulated in human HCC cell lines. MTT assay showed that over-expression of HDAC5 promoted cell proliferation in human HCC cell lines. Down-regulation of HDAC5 caused a significantly inhibition of liver cancer cells proliferation. Furthermore, we found that HDAC5 promoted the Six1 expression both at the mRNA and protein levels in HCC cell lines. CONCLUSIONS: The current study demonstrated for the first time that HDAC5 promoted HCC cell proliferation through up-regulation of Six1 expression and might provide novel therapeutic targets in the treatment of HCC.
OBJECTIVES: Histone deacetylases (HDACs) plays important roles in the regulation of genes expression and contribute to the growth of cancer cells. The present study aimed to investigate the function of HDAC5 in humanhepatocellular carcinoma (HCC). PATIENTS AND METHODS: The expression of HDAC5 in humanhepatocellular carcinoma tissues and cells was detected. MTT assay was used to measure the proliferation of HCC cell lines. siRNA technology was employed to down-regulate the protein expression of HDAC5 and Six1. RESULTS: Western blot showed that the HDAC5 expression was increased in human HCC tissues. The mRNA and protein levels of HDAC5 were up-regulated in human HCC cell lines. MTT assay showed that over-expression of HDAC5 promoted cell proliferation in human HCC cell lines. Down-regulation of HDAC5 caused a significantly inhibition of liver cancer cells proliferation. Furthermore, we found that HDAC5 promoted the Six1 expression both at the mRNA and protein levels in HCC cell lines. CONCLUSIONS: The current study demonstrated for the first time that HDAC5 promoted HCC cell proliferation through up-regulation of Six1 expression and might provide novel therapeutic targets in the treatment of HCC.