Microarray analysis of GFP-SAS cells treated with siAURKA and MLN8237
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ABSTRACT: 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: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:Transcriptional profiling of SAS cells transfected with pLKO.1-LYRIC shRNA-B expression vector (desinaged as B) and control SAS cells (transfected with pLKO.1 vector, designated as CTL). Goal was to determine the effects of LYRIC knockdown on global SAS cells gene expression. Two-condition experiment, SAS cells transfected with pLKO.1-LYRIC shRNA-B expression vector (desinaged as B) v.s. control SAS cells (transfected with pLKO.1 vector, designated as CTL). Biological replicates: 4 control replicates, 4 transfected replicates.
Project description:Stable clones of RPE-1 cells expressing tetracycline-inducible wild type SAS-6 or SAS-6ND were obtained via lentiviral gene transduction with the pLVX tet-on Advanced inducible gene expression system (Clontech). Stable expressors were derived by selection with 5 μg/mL puromycin (Sigma-Aldrich, UK). Doxycycline 1 microgram/mL was added to growth media for 6 days to induce SAS-6 expression. RNA was isolated from RPE-1 cells using the RNeasy mini kit (Qiagen, CA) according to the manufacturer’s protocol. Gene expression was profiled using GeneChip™ Human Transcriptome Array 2.0.
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: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.
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:Whole-genome expression studies in peripheral tissues of patients affected by schizophrenia (SCZ) can provide new insights into the molecular basis of the disorder and innovative biomarkers that may be of great usefulness in the clinical practice. Recent evidence suggests that skin fibroblasts could represent a non-neural peripheral model useful to investigate molecular alterations in psychiatric disorders. A microarray expression study was conducted comparing transcriptomic profiles of skin fibroblasts from SCZ patients and controls. Fibroblasts can be more advantageous to discover mental disorder aetiological mechanisms since they seem more similar to neurons and less affected by the environmental confounders. Transcriptomic profiles of human skin fibroblasts obtained from 20 schizophrenia patients were compared to 20 controls
Project description:Transcriptional profiling of SAS cells transfected with pLKO.1-LYRIC shRNA-B expression vector (desinaged as B) and control SAS cells (transfected with pLKO.1 vector, designated as CTL). Goal was to determine the effects of LYRIC knockdown on global SAS cells gene expression.
Project description:Transcriptional profiling of SAS cells comparing siC-transfected SAS cells with siD-transfected SAS cells. The latter decreased proliferation and migration of SAS cells. Goal was to determine the DDX3-regulated transcripts.
Project description:This study uses RNA-seq analysis to explore the impact of KDM4C, a histone lysine demethylase, on head and neck squamous cell carcinoma (HNSCC). KDM4C modifies histone proteins by removing methyl groups from H3K9me3/2, which affects gene expression. The study focuses on the role of KDM4C in SAS cells, a type of HNSCC cell line, specifically concerning metastasis. Gene Set Enrichment Analysis analyzed RNA-seq data comparing SAS cells with and without KDM4C depletion (sh4C#1 vs. LKO). The result showed that KDM4C significantly influences various metabolic processes, including heme metabolism, peroxisome function, and bile acid metabolism in SAS cells. Additionally, the study performed a KDM4C-ChIP seq analysis on SAS cells to gain further insight into its role. According to Enrichr analysis, GATA1 was the top-ranking transcription factor in these pathways, suggesting its potential interaction with KDM4C in HNSCC.