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Transcriptomes of SIX1 deficient and control Rhabdomyosarcoma cells

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE173150 | GEO | 2022/02/07

REPOSITORIES: GEO

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Chromatin states and transcription factor binding in SIX1 deficient Rhabdomyosarcoma cells

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.

2022-02-07 | GSE173151 | GEO

miRNA expression profiling in rhabdomyosarcoma cell lines

Project description:Rhabdomyosarcomas (RMS) are rare but very aggressive tumours of childhood that arise as a consequence of regulatory disruption of the growth and differentiation pathways of myogenic precursor cells. Based on morphology, two major RMS subtypes can be identified: embryonal RMS (ERMS) and alveolar (ARMS). To better understand the global function of miRNA in RMS, we analyzed the expression profile of 8 different RMS cell lines (3 PAX3/FOXO1 positive and 5 PAX3/FOXO1 negative RMS) using the mirVana miRNA Probe Set V1 (Ambion). The miRNA microarray platform was able to distinguish PAX3/FOXO1 positive (RH4, RH30, RH28) and negative RMS (RD, CCA, SMS-CTR, RH36, RH18) cell lines through the expression pattern of about 90 miRNAs. Since the translocation positive RMS patients fared worse than the negative counterpart our results demonstrated the potential of miRNA expression profiling to classify different RMS subtypes, in agreement to previous gene expression studies, and set the basis for a further functional characterization of selected miRNAs implicated in RMS pathogenesis and in the different clinical behaviour and aggressiveness of the two RMS subtypes. We decided to study miRNAs with the greatest difference in expression between PAX3/FOXO1 positive and negative RMS:miR-23a, miR-27a and miR-199a.

2015-05-04 | GSE52677 | GEO

Genome-wide mapping of CASZ1 binding sites in differentiated SMS-CTR cells [Trametinib]

Project description:MEK inhibitor trametinib induces SMS-CTR cell differentiation and up-regulates CASZ1 expression. We identified genome-wide binding sites of CASZ1 in differentiated SMS-CTR cells.

2019-12-26 | GSE126143 | GEO

Differentially expressed miRNAs in TGF-M-NM-21-knock down rhabdmyosarcoma cell lines vs controls

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.

2012-09-13 | E-GEOD-40843 | biostudies-arrayexpress

Investigate the affect of CASZ1b on chromatin accessibility in SMS-CTR cells

Project description:In SMS-CTR cells, the overexpression of CASZ1b in SMS-CTR cells led to a modification of regional chromation accessibility.

2019-12-26 | GSE126140 | GEO

SNAIL is a key regulator of rhabdomyosarcoma progression and myogenic differentiation

Project description:Rhabdomyosarcoma (RMS) is a frequent non-epithelial tumor of soft tissue that originates from a myogenic differentiation defect. Expression of SNAIL transcription factor is elevated in the alveolar subtype of RMS, characterized by a low myogenic differentiation status and high aggressiveness. SNAIL affects RMS metastasis by reorganization of actin cytoskeleton, regulation of ezrin expression and chemotaxis to HGF and SDF-1. The differentiation of human RMS diminishes SNAIL level. SNAIL silencing completely abolishes the growth of human RMS xenotransplants. SNAIL inhibits myogenic differentiation of RMS by binding to the MYF5 promoter, suppressing its expression, displacing MYOD from canonical to alternative E-box sequences and regulating myomiRs expression. SNAIL silencing allows the re-expression of MYF5 and canonical MYOD binding, promoting RMS cell myogenic differentiation. These novel results open potential avenues for the development of innovative therapeutic strategies based on SNAIL silencing.

2020-07-14 | PXD006711 | Pride

Genome-wide mapping of CASZ1b binding sites and investigate its effect on chromatin status in SMS-CTR cells [CTRtetCASZ1b]

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.

2019-12-26 | GSE126142 | GEO

Microarray Expression Analysis of SIV infection of Sooty Mangabeys

Project description:Natural SIV infection of sooty mangabeys (SMs) does not progress to disease despite chronic virus replication. In contrast to pathogenic SIV infection of rhesus macaques (RMs), chronic SIV infection of SMs is characterized by low immune activation. To elucidate the mechanisms underlying this phenotype, we longitudinally assessed host gene expression in SIV-infected SMs and RMs. We found that acute SIV infection of SMs is consistently associated with a robust innate immune response, including widespread up-regulation of interferon-stimulated genes (ISGs). Our findings indicate that active immune regulatory mechanisms, rather than intrinsically attenuated innate immune responses, underlie the low immuneactivation of chronically SIV-infected SMs. We infected 5 SMs with SIVsmm and assessed their gene expression in RNA derived from whole blood at 3,7,10,14,30 and 180 days post-infection using Rhesus Affymetrix GeneChips. As a comparison, we also analyzed gene expression in 4 RMs infected with SIVsmm, and 8 RMs infected with SIVmac239, a classical pathogenic SIV.

2010-03-08 | E-GEOD-16147 | biostudies-arrayexpress

Differentiation resistant HPV16-immortalized keratinocytes: Six1 transfected vs. Control.

Project description:The overexpression of Six1, a member of the Six family of homeodomain transcription factors, has been found in various human cancers, and is associated with tumor progression and metastasis. We previously determined that the expression of Six1 mRNA increased during in vitro progression of human papillomavirus type 16 (HPV16)-immortalized human keratinocytes (HKc/HPV16) toward a differentiation-resistant (HKc/DR) phenotype. However, if Six1 promotes HPV16-mediated transformation or not remains unknown. HKc/DR were transfected with a Six1 or control vector and RNA isolated from these cells were used in an Agilent two-color gene expression profiling experiment. The goal was to determine the effects of Six1 on global gene expression. Two-condition experiment, Six1 vs. Control HKc/DR cells. Biological replicates: 4 Six1-transfected replicates and 4 control-transfected replicates.

2013-12-24 | E-GEOD-53589 | biostudies-arrayexpress

The BAF complex blocks Myogenesis in rhabdomyosarcoma

Project description:Rhabdomyosarcoma (RMS) is a highly malignant pediatric cancer of skeletal muscle lineage. The aggressive alveolar subtype is commonly characterized by t(2;13) or t(1;13) translocations with the expression of PAX3- or PAX7-FOXO1 fusion transcription factors respectively and is known as fusion positive RMS (FP-RMS). FP-RMS tumors rely on the fusion gene to maintain their proliferative state while avoiding terminal differentiation program. Since disruptions of normal development are likely governed by epigenetic changes in these low-mutational-burden tumors, we investigated the contributions of chromatin regulatory complexes to RMS tumor maintenance. We demonstrate the essentiality of the mSWI/SNF ATPase BRG1 for FP-RMS proliferation and discover that RMS significantly overexpress SMARCA4 (encoding BRG1) compared to skeletal muscle. We define the mSWI/SNF subunit repertoire in FP-RMS and provide evidence for the assembly of multiple mSWI/SNF complexes including canonical BAF, PBAF and non-canonical (nc)BAF in FP-RMS. Proteomic studies suggest proximity between PAX3-FOXO1 and BAF complexes, which was further supported by genome-wide binding profiles revealing enhancer colocalization of BAF with FP-RMS core regulatory transcription factors. We report that mSWI/SNF complexes act as sensors of chromatin state, which are recruited to sites of de novo histone acetylation. Phenotypically, interference with mSWI/SNF complex function induces transcriptional activation of the skeletal muscle differentiation program associated with MYCN enhancer invasion at myogenic target genes. Finally, BRG1 targeting compounds reproduce the effects of genetic ablation. We conclude that inhibition of BRG1 overcomes the differentiation blockade of FP-RMS cells and may provide a therapeutic strategy for treating this lethal childhood tumor.

2020-11-20 | MSV000086494 | MassIVE

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