Project description:Heat shock transcription factor 1 (HSF1) is recognized as the major regulator of the heat shock transcriptional response, and also plays a central role in the cellular functions of cancer cells. Here, to identify the molecular mechanism by which HSF1 regulates the proliferation of cancer cells, comparative gene expression analysis was performed with mock and HSF1-knockdown cells. Silencing of HSF1 in human oral squamous cell carcinoma HSC-3 cells was carried out by siRNA technology and the expression of HSF1 was confirmed by Western blotting. Gene expression was analyzed using GeneChip oligonucleotide microarrays and computational gene expression analysis tools. HSF1 knockdown significantly decreased the number of viable cells. Of the 54,675 probe sets analyzed, 221 probe sets were up-regulated and 423 probe sets were down-regulated by >2-fold in HSF1-knockdown cells. HSC-3 human oral squamous carcinoma cells were treated with siRNA for HSF1 or luciferase. Total RNA samples were prepared from the cells. Gene expression was analyzed by an Affymetrix GeneChipM-BM-. system with a Human Genome U133-plus 2.0 array. Sample preparation for array hybridization was carried out as described in the manufacturerM-bM-^@M-^Ys instructions.
Project description:To unravel the function of VAMP7 in the male sexual differentiation, we carried out in vitro studies of VAMP7 knockdown using siRNA, in the human embryonal carcinoma NTERA2/D1 cells.
Project description:To investigate the phenotypic consequences of PLVAP presence/absence in human LSEC, we utilised siRNA knockdown in 3 independent LSEC donors. We then performed gene expression profiling analysis using data obtained from RNA-seq of LSEC with siRNA knockdown of PLVAP and siRNA Negative Control cells.
Project description:Quantification of lipid species from cultured human MDA-MB-231 and BT549 cells with or without siRNA knockdown of ACSL1 and treated or not with eleostearic acid
Project description:Rho-GTPases are small GTP-binding proteins that contribute to the epithelial-to-mesenchymal transition by regulating several cellular processes including organization of the actin cytoskeleton, cell motility, transcription, and cell proliferation. Overexpression of RhoC-GTPases (RhoC) in breast cancer has been implicated in poor disease prognosis due to increased cancer cells invasion, migration, and motility, which warranted its consideration as a therapeutic target for inhibiting breast cancer metastasis. Using silencing RNA (siRNA) molecules to knockdown RhoC expression is a promising approach to inhibit breast cancer metastases.
Project description:Transcriptional profiling of human embryo kidney cells comparing control HEK293 transfected with empty vectors cells with HEK293 cells transfected with pcDNA3-ZNF191 (or ZNF191 siRNA vector). We searched for early ZNF191 target genes by using a transient overexpression and knockdown strategy in the human embryo kidney (HEK293) cells. A table of gene targets of transcription factor ZNF191 commonly identified by both strategies is appended below as a supplementary file.
Project description:To examine the effects of SRp20 on genome-wide RNA splicing in tumor cells, we utilized Exonhit SpliceArray to compare genome-wide changes of RNA splicing and transcription in U2OS cells with or without knockdown of SRp20 by RNAi. U2OS cells were treated by SRp20 siRNA or non-specific siRNA, each performed in triplicate. A human genome-wide splice-array assay was performed by using a service provider ExonHit Therapeutics, Inc (Gaithersburg, MD). Fifty ng of total RNA isolated from U2OS cells with or without knockdown of SRp20 was quality controlled and analyzed by using Affymetrix GeneChip platform to profile the expression of 20,649 genes and splicing events of 19,066 genes.
Project description:The Hypoxia-Inducible Factors induce the expression of the histone demethylases JMJD1A (KDM3A) and JMJD2B (KDM4B), linking the hypoxic tumor microenvironment to epigenetic mechanisms that may foster tumor progression. Using transcript profiling, we have identified genes that are regulated in RCC4 with siRNA-mediated knockdown of JMJD1A and JMJD2B. This dataset includes expression data obtained from renal cell Carcinoma being loss or mutation of the von Hippel-Lindau (VHL) tumor suppressor gene combination with siRNA-mediated knockdown of histone demethylases JMJD1A and JMJD2B.