Project description:In SMS-CTR cells, we identified genomewide binding sites of CASZ1b. The overexpression of CASZ1b in SMS-CTR cells led to a regional epigenetic modification.
Project description:Genetic and shRNA-mediated inhibition of SIX1 expression in RMS cells induces myogenic differentiation and impedes RMS tumor growth. To elucidate the mechanism by which SIX1 loss activates a differentiation program, we performed SIX1, MYOD1, and H3K27ac ChIPseq in two SIX1 knockdown SMS-CTR cell lines and one control SMS-CTR cell line to profile changes in transcriptional activity and myogenic transcription factor binding in fusion-negative Rhabdomyosarcoma.
Project description:To investigate the role of TGF-M-NM-21-regulated miRNAs in the progression of RMS,we performed comprehensive miRMA microarray analysis on RNA derived from typical RMS cell lines and TGF-M-NM-21 knock-down cell lines. We identified a novel set of TGF-M-NM-21-related miRNAs. Total RNA was isolated from TGF-M-NM-21-knock down rhabdmyosarcoma cell lines and controls. Three-condition experiment: shRNA-TGF-M-NM-21/RD cells vs. shRNA-Control/RD cells, shRNA-TGF-M-NM-21/SMS-CTR cells vs. shRNA-Control/ SMS-CTR cells, and shRNA-TGF-M-NM-21/RH28 cells vs. shRNA-Control/RH28 cells. Biological replicates: 1 RD cells stably transfected with shRNA-TGF-M-NM-21- pSUPER gfp-neo, 1SMS-CTR cells stably transfected with shRNA-TGF-M-NM-21- pSUPER gfp-neo, 1RH28 cells stably transfected with shRNA-TGF-M-NM-21- pSUPER gfp-neo, 1RD cells stably transfected with shRNA-Control- pSUPER gfp-neo, 1SMS-CTR cells stably transfected with shRNA-Control- pSUPER gfp-neo, and 1RH28 cells stably transfected with shRNA-Control- pSUPER gfp-neo, independently grown and harvested. One replicate per array.
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare NGS-derived retinal transcriptome profiling (RNA-seq) to microarray and quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods and to evaluate protocols for optimal high-throughput data analysis Genetic and shRNA-mediated inhibition of SIX1 expression in RMS cells induces myogenic differentiation and impedes RMS tumor growth. To elucidate the mechanism by which SIX1 loss activates a differentiation program, we performed RNAseq in two SIX1 knockdown SMS-CTR cell lines and one control SMS-CTR cell line to profile changes in transcriptome.