Project description:H3K27me3 ChIP-seq was performed on: 1) untreated SH-SY5Y human neuroblastoma cells (day 0) 2) vincristine-treated SH-SY5Y human neuroblastoma cells (7 days of treatment - day 7) 3) vincristine-treated SH-SY5Y human neuroblastoma cells (7 days of treatment + 7 days of recover - day 14)
Project description:We perturbed the expression levels of circSLC45A4 in the human neuroblastoma cell line (SH-SY5Y) by RNAi/siRNAs. 96 h post-knockdown the cells were harvested, RNA extracted with Trizol and polyA+ libraries were generated with Illumina's TruSeq RNA Library Prep Kit v2. We find many significant changes in the transcriptomic profile after knockdown of circSLC45A4 and the induction of many genes connected to nervous system development, neuron projection development, synapse organization and cell adhesion.
Project description:The goal of this study was to identify dynamic changes in signaling pathway activities after KIT knockdown by RNAi in neuroblastoma with relatively high KIT expression (SH-SY5Y) and low expression (SK-N-AS).
Project description:The RNA-binding protein hnRNP K was knocked down using siRNA in human SH-SY5Y. As a control, cells were treated with an siRNA against firefly luciferase.
Project description:Background: SH-SY5Y cells exhibit a neuronal phenotype when treated with all-trans retinoic acid (RA), but the molecular mechanism of activation in the signaling pathway mediated by phosphatidylinositol 3-kinase (PI3K) is not sufficiently understood. To shed new light on the mechanism, we comprehensively compared the gene expression profiles between SK-N-SH cells and two subtypes of SH-SY5Y cells (SH-SY5Y-A and SH-SY5Y-E), each of which showed a different phenotype during RA-mediated differentiation. Results: SH-SY5Y-A cells differentiated in the presence of RA, whereas RA-treated SH-SY5Y-E cells required additional treatment with brain-derived neurotrophic factor (BDNF) for full differentiation. In combination with perturbation using a PI3K inhibitor, LY294002, we identified 386 genes and categorized them into two clusters dependent on the PI3K signaling pathway during RA-mediated differentiation in SH-SY5Y-A cells. Transcriptional regulation of the gene cluster was greatly reduced in SK-N-SH cells or partially impaired in SH-SY5Y-E cells in coincidence with a defect in the neuronal phenotype of these cell lines. Additional stimulation with BDNF induced a set of neural genes which were down-regulated in RA-treated SH-SY5Y-E cells but were abundant in the differentiated SH-SY5Y-A cells. Conclusions: We identified the gene clusters controlled by PI3K- and TRKB-mediated signaling pathways during differentiation in two subtypes of SH-SY5Y cells. TRKB-mediated bypass pathway compensates for the impaired neural functions generated by defects in several signaling pathways including PI3K in SH-SY5Y-E cells. The expression profiling data are useful for further studies to elucidate the signal transduction-transcriptional network including PI3K and/or TRKB. Keywords: Cell type comparison, time course
Project description:The SH-SY5Y Human neuroblastoma cell line was subcloned from the SK-N-SH cell line, which has been isolated from a bone marrow biopsy of a 4 year-old female patient. To examine the overall distribution of gene expression under stress condition in human neuronal cells, we investigated changes in the transcriptome profiles in the SH-SY5Y cells depleted with ERRαlpha and ERRgamma by gene knockdown. We detected changes in the expression levels for several genes.
