ChIP-seq analysis of SNAIL transcription factor binding sites in RH30 rhabdomyosarcoma cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA639097 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12004247_1.fastq.gz | Fastqsanger.gz | |||
| SRR12004247_2.fastq.gz | Fastqsanger.gz | |||
| SRR12004248_1.fastq.gz | Fastqsanger.gz | |||
| SRR12004248_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 4 of 4 |
Similar Datasets
Project description:ChIP-seq analysis of SNAIL binding sites in RH30 cells was performed to discover novel SNAIL binding sites in rhabdmyosarcoma cells.
2020-07-15 | GSE152355 | GEO
Project description:The main goal of the project was to analyze the effect of SNAIL transcription factor on microRNA expression profile in rhabdomyosarcoma (RMS) cells using the next generation sequencing. Differential expression of microRNAs between three groups was compared in RH30 alveolar RMS cells: WT (WT), shCTRL (modified with control shRNA vector) and shSNAIL (modified with shRNA against SNAIL). Different groups were compared to investigate the effect of SNAIL silencing on microRNA up- or downregulation.
2020-07-15 | GSE100114 | GEO
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
Project description:The effect of the Smac mimetic BV6 on the transcriptional regulation in the alveolar rhabdomyosarcoma cell line RH30 was investigated by bulk RNA-sequencing. To this end, RH30 cells were treated with 5 µM BV6 for 24 h, or left untreated. Here, a regulation of several NF-κB target genes could be observed.
2023-04-04 | GSE223787 | GEO
Project description:We report the genome-wide maps of PAX3-FKHR binding sites. Chromatin immunoprecipitation was performed against PAX3-FKHR positive (Rh4) and PAX3-FKHR negative (RD) rhabdomyosarcoma cells with a monoclonal antibody (pFM2) specific for the fusion region of PAX3-FKHR. We obtained 4 million sequence tags for both input and ChIP DNA that aligned to the human genome. We identified 1,463 binding sites from ChIP-seq of Rh4 cells, none of which appeared from ChIP-seq of fusion negative RD cells. The PAX3-FKHR binding sites were found to associate with 1,072 genes in RMS cells. The data shows that PAX3-FKHR binds to the same sites as PAX3, at the enhancers for MYF5, FGFR4, and the MYOD core enhancer previously shown to be regulated by PAX3. Moreover, our dataset has the precision for rapid identification and validation of novel and specific sequences required for the enhancer activity of MYOD and FGFR4. The genome wide analysis reveals that the PAX3-FKHR sites are: 1) mostly distal to transcription start sites; 2) conserved; 3) enriched for PAX3 motifs; and 4) strongly associated with genes over-expressed in PAX3-FKHR positive RMS cells and tumors. There is little evidence in our dataset for PAX3-FKHR binding at the promoters. In one instance, we show two intronic enhancer elements for MET, rather than at the previously described promoter. The genome-wide analysis further illustrates a strong association between PAX3 and E-box motifs in these binding sites, suggestive of a common co-regulation for many target genes. The map of PAX3-FKHR binding sites provides new links for PAX3 and PAX3-FKHR functions and new targets for RMS therapy. Examination of PAX3-FKHR binding sites in translocation-positive rhabdomyosarcoma cells via ChIP-seq with an antibody specific for the fusion protein.
2010-08-17 | E-GEOD-19063 | biostudies-arrayexpress
Project description:The objective was to identify the molecular mechanisms responsible for in vitro and in vivo efficacy of an anti-MYCN peptide nucleic acid on a preclinical model of alveolar rhabdomyosarcoma. Cells treated with a anti-MYCN PNA exhibit growth arrest and apoptosis, and in vivo tumor growth is blocked. Keywords: oncogene inhibition RH30 alveolar rhabdomyosarcoma cell line was treated with a 10uM concentration of anti-MYCN PNA or a mutated PNA devoid of any activity. After 12 hours RNA was extracted from untreated and treated cells and gene expression was analyzed by Affymetrix Gene Chips.
2011-12-31 | E-GEOD-7959 | biostudies-arrayexpress
Project description:The purpose of our study was to examine the function of BMI1 in fusion positive and fusion negative rhabdomyosarcoma cell lines and validate these findings in patient tissue. RD and RH30 cell lines were treated with control-siRNA or BMI1-siRNA and the RNA was subsequently sequenced on a HiSeq2500. The resultant sequencing data was used for Gene Set Enrichment Analysis and pathway analysis.
2016-12-20 | E-MTAB-4237 | biostudies-arrayexpress
Project description:Classical NF-κB activity can be inhibited by overexpression of the IκBα super repressor (SR). To determine the role of NF-κB in rhabdomyosarcoma cells, we overexpressed the IκBα SR in RH30 rhabdomyosarcoma cells. IκBα SR was overexpressed in RH30 cells. RH30 vector cells were used as control group.
2018-03-30 | GSE112119 | GEO
Project description:Background: Alveolar rhabdomyosarcoma (ARMS) has a high propensity to metastasize, leading to its aggressiveness and a poor survival rate among those with the disease. More than 80% of aggressive ARMSs harbor a PAX3-FKHR fusion transcription factor, which regulates cell migration and promotes metastasis, most likely by regulating the fusion protein's transcriptional targets. Therefore, identifying druggable transcription targets of PAX3-FKHR that are also downstream effectors of PAX3-FKHR-mediated cell migration and metastasis may lead to novel therapeutic approaches for treating ARMS. Methods: To identify genes whose expression is directly affected by the level of PAX3-FKHR in an ARMS cellular-context, we first developed an ARMS cell line in which PAX3-FKHR is stably down-regulated, and showed that stably downregulating PAX3-FKHR in ARMS cells significantly decreased the cells' motility. We used microarrays analysis to identify genes whose expression level decreased when PAX3-FKHR was downregulated. We used mutational analysis, promoter reporter assays, and electrophoretic mobility shift assays to determine whether PAX3-FKHR binds directly and specifically to the promoter region of the target gene. We used siRNA and pharmacologic inhibitor to downregulate the target gene of PAX3-FKHR and investigated the effect of such downregulation on cell motility, Results: We found that When PAX3-FKHR was downregulated, the expression of carnitine palmitoyltransferase 1A (CPT1A) decreased. We showed that PAX3-FKHR binds directly and specifically to a paired-domain binding-site in the CPT1A promoter region, indicating that CPT1A is a novel direct transcriptional target of PAX3-FKHR. Furthermore, downregulating CPT1Adecreased cell motility in ARMS cells, indicating that CPT1A is a downstream effector of PAX3-FKHR-mediated cell migration and metastasis. Conclusions: Taken together, we have identified CPT1A as a novel direct transcriptional target of PAX3-FKHR and revealed the novel function of CPT1A in promoting cell motility. CPT1A may represent a novel therapeutic target for the treatment of ARMS. Identification of transcription targets of PAX3-FKHR in human alveolar rhabdomyosarcoma: By stably knocking down PAX3-FKHR in human alveolar rhabdomyosarcoma cell line Rh30 and comparing the gene expression profile of the knockdown clone (KD) to the parental Rh30, transcription targets of PAX3-FKHR have been identified. Gene expression in parental Rh30 cells was compared to that in either Rh30 cells stably expressing shRNA targeting PAX3-FKHR (KD) or control non-targeting shRNA (CON), in duplicate.
2012-05-15 | E-GEOD-35862 | biostudies-arrayexpress
Project description:Purpose: Our laboratory has recently reported novel tumor-suppressive roles of PANX1 in both embryonal (eRMS) and alveolar (aRMS) rhabdomyosarcoma, but the underlying molecular mechanism remains to be elucidated. Methods: PANX1-induced differential gene expression profile in alveolar rhabdomyosarcoma (RMS) cell line, Rh30, was generated by deep sequencing using Illumina HiSeq2000. The sequence reads that passed quality filters were analyzed by BOWTIE/TOPHAT pipeline with accessary programs SAMTOOLS (v1.0) and CUTADAPT (v1.7.1) followed by Cufflinks (v2.2.1). The protein expression of the differentially regulated genes was validated by Western blotting. Results: Using RNA-seq and DAVID analysis, we showed that the Gene Ontology (GO) terms such as apoptosis and migration, and KEGG pathways such as MAPK and Rap1 Signaling pathways were amongst the most highly enriched processes in Rh30 (aRMS) cells with ectopic PANX1 expression. We found that both GJA1 and its encoded protein connexin 43 (Cx43) were significantly increased in PANX1 expressing Rh30 (aRMS) cells. Conclusion: PANX1 transcriptome and proteome databases hold great potential for discovery of novel PANX1 tumor-suppressive mechanisms and therapeutic targets for RMS.
2021-01-22 | GSE144102 | GEO