Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Quantitative assessment of transcriptomic differences between ASPcKO and ASPcKOP7cKO flow cytometry-sorted murine FN-RMSs by RNA sequencing

ABSTRACT: We report the transcriptomic differences between ASPcKO and ASPcKOP7cKO flow cytometry-sorted FN-RMSs by RNA sequencing. The goal of this study is to determine what role Pax7 loss has on Pten-deficient, Hedgehog-activated murine FN-RMS tumors. These results provide implications for the transcriptomic program driven by Pax7 in dictating FN-RMS tumor fate.

ORGANISM(S): Mus musculus

PROVIDER: GSE166808 | GEO | 2021/08/24

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Differences in gene expression between ASP WT and ASPcKO tumors

Project description:To further examine the consequences of Pten loss in a Hedgehog driven, murine FN-RMS, we used microarrays to determine the transcriptomic differences between our aP2-Cre;SmoM2 FN-RMS model (Hatley et al. 2012, Cancer Cell) and aP2-Cre; SmoM2; Pten flox/flox FN-RMSs.

2021-08-24 | GSE166809 | GEO

TWIST2-Mediated Chromatin Remodeling Promotes Fusion-Negative Rhabdomyosarcoma [RNA-seq FN-RMS Cells]

Project description:Sarcomas are derailed in pathways that specify mesenchymal lineages during embryogenesis, causing tumor cells to stall at early stages of differentiation. Among them, rhabdomyosarcoma (RMS) is a pediatric soft tissue sarcoma of skeletal muscle origin. A key feature of RMS is their inability to terminally differentiate despite the high expression of master myogenic regulator MYOD. The bHLH transcription factor TWIST2, which governs mesenchymal stem cell identity and restricts myogenesis, is overexpressed in patient fusion-negative RMS (FN-RMS) tumors. We show that knockdown of TWIST2 enables FN-RMS cells to exit the cell cycle and undergo myogenic differentiation, thereby reducing the growth of FN-RMS xenograft tumors. ChIP-seq analysis revealed that most TWIST2-mediated gene regulation occurs independent of changes in MYOD binding in FN-RMS cells. Instead, TWIST2 controls the deposition of H3K27 acetylation at distal enhancers by interacting with the chromatin remodelers, SMARCA4 and CHD3, to activate growth-related and repress myogenesis-related TWIST2 target genes. Our findings provide new insights into the role of TWIST2 in maintaining an undifferentiated and tumorigenic state of FN-RMS and highlight the clinical potential of reversing the TWIST2-regulated phenotype.

2023-03-20 | GSE207167 | GEO

Transcriptomic changes in SJRHB015721_X1 human FN-RMS following DBX1 knock-down

Project description:DBX1 is a transcriptional repressor whose role in human cancer is poorly understood. DBX1 is highly expressed in FN-RMS. Here, we depleted DBX1 expression with 2 shRNAs targeting DBX1 in a human FN-RMS cell line we derived from a PDX - SJRHB015721_X1. We determined the transcriptional changes using a Clariom S human microarray.

2021-08-24 | GSE166810 | GEO

Quantitative assessment of transcriptomic differences between ASPcKO and ASPcKOP7cKO flow cytometry-sorted murine FN-RMSs by RNA sequencing

Project description:Quantitative assessment of transcriptomic differences between ASPcKO and ASPcKOP7cKO flow cytometry-sorted murine FN-RMSs by RNA sequencing

| PRJNA702052 | ENA

Rhabdomyosarcoma surfaceome profiling with six fusion-positive (FP) RMS cell lines, five fusion-negative (FN) RMS cell lines, and three ARMS patient-derived xenografts (PDXs)

Project description:Rhabdomyosarcoma (RMS) is the most common soft tissue sarcoma in children. Prognosis for patients with high grade and metastatic disease is still very poor, and survivors are burdened with long-lasting side effects. Therefore, more effective and less toxic therapies are needed. Surface proteins are ideal targets for antibody-based therapies, like bispecific antibodies, antibody drug conjugates, or chimeric antigen receptor (CAR) T cell. Specific surface targets for RMS are scarce. Here, we performed a surfaceome profiling based on differential centrifugation enrichment of surface/membrane proteins and detection by LC-MS on six fusion-positive (FP) RMS cell lines, five fusion-negative (FN) RMS cell lines, and three RMS patient-derived xenografts (PDXs). 699 proteins were detected in the three RMS groups. Ranking based on expression levels and comparison to expression in normal MRC-5 fibroblasts and myoblasts, followed by statistical analysis, highlighted known RMS targets such as FGFR4, NCAM1, and CD276/B7-H3, and revealed AGRL2, JAM3, MEGF10, GPC4, CADM2, as potential targets for immunotherapies of RMS. L1CAM expression was investigated in RMS tissues and strong L1CAM expression was observed in more than 80% of alveolar RMS tumors, making it a practicable target for antibody-based therapies of alveolar RMS.

2023-03-11 | PXD039480 | Pride

Deep Sequencing the microRNA profile in rhabdomyosarcoma reveals down-regulation of miR-378 family members

Project description:Rhabdomyosarcoma (RMS) is a highly malignant tumour accounting for nearly half of soft tissue sarcomas in children. Altered miRNA levels have been reported in human cancers, including RMS. Using deep sequencing technology, a total of 685 miRNAs were investigated in a group of alveolar RMSs (ARMSs), embryonal RMSs (ERMSs) as well as in normal skeletal muscle (NSM). Bioinformatics pipelines were used for miRNA target prediction and clustering analysis. Ninety-seven miRNAs were significantly deregulated in ARMS and ERMS when compared to NSM. MiR-378 family members were dramatically decreased in RMS tumour tissue and cell lines. Interestingly, members of the miR-378 family presented as a possible target the insulin-like growth factor receptor 1 (IGF1R), a key signalling molecule in RMS.

2015-01-28 | E-MTAB-3246 | biostudies-arrayexpress

Transcriptome analysis of genetically engineered murine fusion-negative rhabdomyosarcoma model-derived cell lines

Project description:Fusion-negative rhabdomyosarcoma (FN-RMS) is the most common soft tissue sarcoma of childhood arising from undifferentiated skeletal muscle cells. Tumor cells derived from genetically engineered murine models are a valid tool to study cancer biology. In order to investigate the poor myogenic commitment of FN-RMS, we performed RNA sequencing of two cell lines derived from a previously described genetically engineered murine model of FN-RMS. We then performed bioinformatics analysis to compare the transcriptome with murine satellite cells, and identify the key factors that distinguish FN-RMS from skeletal muscle cells.

2021-05-31 | GSE175816 | GEO

Effect of Fusobacterium nucleatum (Fn) infection or Fn-Dps treatment on gene expression of esophageal carcinoma Kyse150 and Kyse30 cells

Project description:Kyse150 and Kyse30 cells were infected by Fn (the MOI of 1:10) or treated with Fn-Dps (1 μM) for 48 h

2023-06-01 | GSE222917 | GEO

The Fusobacterium Nucleatum (Fn) in colorectal carcinogenesis

Project description:To elucidate whether Fusobacterium Nucleatum(Fn) plays a role in colorectal cancer tumorigenesis, a RNA-seq analysis was performed to compare the gene expression profiles of Fn treated HCT116 colorectal cancer cell lines.

2021-02-23 | GSE141805 | GEO

TWIST2-Mediated Chromatin Remodeling Promotes Fusion-Negative Rhabdomyosarcoma [RNA-seq Xenograft]

2023-03-20 | GSE207168 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data