Project description:Knockdown of Akt1 markedly inhibited the growth of GFP-SAS cells. We investigated the molecular mechanisms of the growth inhibitory effect by siAkt1 using Affymetrix GeneAtlasTM System. Using Affymetrix GeneAtlas System, we determined the gene expression profiles of GFP-SAS cells treated with siAkt1 or non-targeting siRNA (siNT).
Project description:Knockdown of Akt1 markedly inhibited the growth of GFP-SAS cells. We investigated the molecular mechanisms of the growth inhibitory effect by siAkt1 using Affymetrix GeneAtlasTM System.
Project description:Inhibition of miR-361-3p by locked nucleic acid (LNA)/DNA antisense oligonucleotide markedly suppressed the growth of GFP-SAS cells. We explored the target genes of miR-361-3p in GFP-SAS cells using microarray analysis.
Project description:To evaluate the effect of OCT1 in breast cancer cells, expression of OCT1 was knocked down in MCF-7 cells by small interfering RNA (siRNA). Microarray analysis was performed to analyze gene expression profiles of these cells.
Project description:To evaluate the effect of TRIM47 on NF-κB signaling in breast cancer cells, expression of TRIM47 was knocked down in MCF-7 cells and its 4-hydroxytamoxifen (OHT)-resistant derivative OHTR cells by small interfering RNA (siRNA). Microarray analysis was performed to analyze gene expression profiles of these cells.
Project description:The expression of clock genes are co-regulated by BMAL1 and CLOCK in all tissue including kidney. Whether these clock-regualted genes can be affected by melatonin still unclaer. To further examine the possible mechanism and biological consequence, we depleted BMAL1 or CLOCK with small interfering RNA (siRNA) and treated cells with melatonin. Then, we used microarray analyses to identify clock genes regulated by melatonin in renal tubular epithelial cell.
Project description:Although galectin-3 is known to modulate the cell proliferation, RNA processing, tumorigenesis, metastasis and apoptosis and also, which is highly expressed in human cancers, the function of galectin-3 is still controversy in gastric cancer. Here, we demonstrated the function of galectin-3 on gastric cancers by silencing with synthetic double-stranded small interfering RNA (siRNA). After silencing of galectin-3, cell numbers decreased and cell shapes changed in round. To determine the mechanism, microarray analysis was used to detect the changes in gene expression by galectin-3 silencing. we silenced galectin-3 in AGS as a gastric cancer cells with synthetic double-stranded small interfering RNA (siRNA), and performed the microarray analysis to detect the changes in gene expression by galectin-3 silencing.
Project description:Knockdown of AURKA by siAURKA and treatment with MLN8237 markedly inhibit the growth of GFP-SAS cells. We investigated the molecular mechanisms of siAURKA and MLN8237 using the Affymetrix GeneAtlasTM System. Using the Affymetrix GeneAtlas System, we compared gene expression profiles of GFP-SAS cells treated with siAURKA, siNon-target (siNT), MLN8237, or DMSO.
Project description:Non-treated, scrambled siRNA (control) and downregulated Edem2 samples were subjected to full gene expression. Ambion® Silencer® Select Pre-designed for rat Edem2 specific small interfering (siRNA) (cat. n. 4390771) and control (siSCR) (cat. n. 4390843) were purchased from (ThermoFisher). Lipofectamine® 2000 was used for transfecting siRNA in Opti-MEM™ Medium according to the manufacturer’s instruction. Edem2 mRNA level at 72 hours post-transfection was suppressed to 7.7% in siRNA cells compared to scrambled cells. The aim of this was to see the expression different when Edem2 was suppressed in normal condition.
