Project description:In order to identify the TSA responsive genes, we performed a gene expression microarray analysis for the RNAs isolated from TSA-untreated and TSA-treated human keratinocytes
Project description:To explore how TSA-MSCexo improves myocardial ischemia-reperfusion injury, miRNA microarray analysis was used to screen differentially expressed miRNAs in MSCexo and TSA-MSCexo.
Project description:To explore TSA influence on human breast cancer cells, we attempt to analyze genes differentially expressed between TSA treated and untreated SKBR3 cells, which will hopefully provide clues for TSA target genes.
Project description:Analysis of MDA-MB-231 cells following TSA treatment or not. TSA regulates various miRNA expression in MDA-MB-231 cells.Results provide insight into the role of miRNAs-involved mechanisms underlying TSA-mediated effects on breast cancer stemness.
Project description:Firstly our study demonstrated that TSA can inhibits cell proliferation, induces cell apoptosis and cell cycle arrest in CCA cell lines in vitro. To identify the target transcripts of TSA to suppress CCA tumorigenesis, mRNA expression profiles were determined by microarray analysis. We chose TFK-1 cells treated by TSA in indicated concentration (IC50) 48 hours for the microarray. Then we found out TACC3 was downregulated, and demonstrated that TACC3 was high expression and may played a role as an target of TSA in inhibiting CCA cells proliferation and migration via in vitro and vivo experiments.
Project description:Histone deacetylase inhibitors (HDACi), such as Trichostatin A (TSA), hold enormous promise for the treatment of HCC. In this study, we investigated the effects of TSA treatment on a c-Myc-induced HCC model in mice. TSA treatment delayed the development of HCC, and liver function indicators such as ALT, AST, liver weight ratio, and spleen weight ratio indicated the effectiveness of TSA treatment. Oil red staining further demonstrated that TSA attenuated lipid accumulation in the HCC tissues of mice. Through mRNA sequencing, we identified that TSA mainly affected cell cycle and fatty acid degradation genes, with alcohol dehydrogenase 4 (ADH4) potentially being the core molecular downstream target. QPCR, immunohistochemistry, and western blot analysis revealed that ADH4 expression was repressed by c-Myc and recovered after TSA treatment both in vitro and in vivo. Furthermore, we observed that the levels of total NAD+ and NADH, NAD+, NAD+/NADH, and ATP concentration increased after c-Myc transfection in liver cells but decreased after TSA intervention. The levels of phosphorylated protein kinase B (p-AKT) and p-mTOR were identified as targets regulated by TSA, and they governed the ADH4 expression and the downstream regulation of total NAD+ and NADH, NAD+, NAD+/NADH, and ATP concentration. Overall, our study suggests that TSA has a therapeutic effect on c-Myc-induced HCC through the AKT-mTOR-ADH4 pathway.
Project description:Haploid embryos can be induced from cultured immature pollen following stress treatment. In Brassica napus, the application of the histone/lysine deacetylase (HDAC/KDAC) inhibitor trichostatin A (TSA) to pollen cultures enhances the production of differentiated embryos and embryogenic callus when applied together with heat stress (Li et al., 2014). To identify genes associated with the induction of haploid embryogenesis and to investigate which genes may be responsible for TSA-induced lipid and starch accumulation in the embryogenic structures, we compared the transcriptomes of pollen cultures treated with heat stress and 0.05 µM TSA to those of untreated pollen cultures, both at two days.
