As a high-cost neurological disability, spinal cord injury (SCI) can result in permanent paralysis and loss of sensation. To identify the temporal genes involved in the pathogenesis of SCI, we analysed the expression profile of GSE45006. GSE45006 was downloaded from Gene Expression Omnibus, including 20 SCI samples (samples at 1 day, 3 days, 1 week, 2 weeks and 8 weeks after injury, four repetitions for each time point) and 4 normal samples. The Bayesian Estimation of Temporal Regulation (BETR) and randomForest packages were used to screen the temporal genes and the top 100 temporal genes, respectively. Then, the gplots package and Pearson correlation analysis separately were used to perform hot map analysis and expression pattern clustering for the top 100 temporal genes. Using the clusterProfiler package and TargetMine tool, their potential functions were analysed by enrichment analyses. Moreover, interaction relationships between these temporal genes and pathways were investigated by pathway–gene crosslinking networks. In total, 1907 temporal genes were identified. The top 100 temporal genes were obtained and divided into six clusters. Most of the gene functions were enriched in biological process categories. ARG1 and NOS3 in cluster 4 were enriched in biological process of arginine catabolic process. TGFβ2, TGFβ3, ALDH2 and ALDH3A2 were correlated with numerous pathways in the pathway–gene crosslinking network. Pathways related to TGFβ2 and TGFβ3 were connected to pathways related to ARG1 and NOS3 via ARG1. Several temporal genes, including TGFβ2, TGFβ3, ALDH2, ALDH3A2, ARG1 and NOS3, might be involved in SCI.

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.