Project description:To clarify the role of miR-186 in GIST, we carried out a gene expression microarray analysis using GIST-T1 cells transfected with a miR-186 inhibitor or a negative control. We found that 253 probe sets (229 unique genes) were upregulated (>1.5-fold) by inhibition of miR-186 in GIST-T1 cells.
Project description:To clarify the effect of miRNAs, we carried out a gene expression microarray analysis using GIST-T1 cells transfected with a miR-335 mimic or a negative control. We found that 1,095 probe sets (853 unique genes) were downregulated (>1.5-fold) by ectopic miR-335 expression. GIST-T1 cells were transfected with a mirVana miR-335 mimic (Ambion) or a mirVana miRNA mimic Negative Control #1 (Ambion). Forty-eight hours after transfection, total RNA extraction was carried out, and gene expression signatures were analyzed.
Project description:To clarify the effect of miRNAs, we carried out a gene expression microarray analysis using GIST-T1 cells transfected with a miR-34a mimic or a negative control. We found that 2,621 probe sets (1,933 unique genes) were downregulated (>1.5-fold) by ectopic miR-34a expression, including PDGFRA gene which was previously reported as a miR-34a target gene. GIST-T1 cells were transfected with a mirVana miR-34a mimic (Ambion) or mirVana miRNA mimic Negative Control #1 (Ambion). Forty-eight hours after transfection, total RNA extraction was carried out, and gene expression signatures were analyzed.
Project description:To clarify the effect of miRNAs, we carried out a gene expression microarray analysis using GIST-T1 cells transfected with a miR-335 mimic or a negative control. We found that 1,095 probe sets (853 unique genes) were downregulated (>1.5-fold) by ectopic miR-335 expression.
Project description:To clarify the effect of miRNAs, we carried out a gene expression microarray analysis using GIST-T1 cells transfected with a miR-34a mimic or a negative control. We found that 2,621 probe sets (1,933 unique genes) were downregulated (>1.5-fold) by ectopic miR-34a expression, including PDGFRA gene which was previously reported as a miR-34a target gene.
2015-05-25 | GSE68740 | GEO
Project description:Gene expression signatures in GIST-T1 cells transfected with miR-34a and miR-335 mimic molecules
Project description:Epigenetic alterations play an important role in the pathogenesis of gastrointestinal stromal tumors (GISTs). To obtain better insight into the GIST epigenome, we analyzed genome-wide histone modification and DNA methylation in GIST cells. Trimethylation of histone H3 lysine 3 (H3K4me3), DNA methylome, and transcriptome in GIST-T1 cells were analyzed by chromatin immunoprecipitation-sequencing (ChIP-seq), Infinium HumanMethylation450 BeacChip, and gene expression microarray. Enrichment of H3K4me3 at transcription start sites (TSSs) is positively correlated with gene expression, while DNA methylation is negatively associated with gene expression in GIST-T1 cells. We found that treatment with a DNA methyltransferase inhibitor and a histone deacetylase inhibitor not only upregulated genes with DNA methylation, but also activated a number of interferon signaling-related genes. ChIP-seq analysis revealed that the drug treatment significantly upregulated H3K4me3 levels at TSS regions as well as retrotransposons including endogenous retroviruses (ERVs). Finally, by utilizing the omics data, we screened epigenetically silenced long non-coding RNA genes, and found that hypermethylation of MEG3 is a frequent event and an indicator of worse outcome in GIST patients. Our data suggest that epigenetic inhibitors may activate interferon signaling via viral mimicry in GIST cells. We also show that epigenome data obtained in this study could be a useful resource to identify novel GIST-related genes.
