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CD73 contributes to the pathogenesis of Fusion-Negative Rhabdomyosarcoma through the purinergic signaling pathway

ABSTRACT: CD73 contributes to the pathogenesis of Fusion-Negative Rhabdomyosarcoma through the purinergic signaling pathway

PROVIDER: PRJNA1004666 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25619045.fastq.gz	Fastqsanger.gz
	SRR25619046.fastq.gz	Fastqsanger.gz
	SRR25619047.fastq.gz	Fastqsanger.gz
	SRR25619048.fastq.gz	Fastqsanger.gz
	SRR25619049.fastq.gz	Fastqsanger.gz

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CD73 contributes to the pathogenesis of Fusion-Negative Rhabdomyosarcoma through the purinergic signaling pathway

Project description:We performed RNA-seq to evaluated the transcriptional changes of CD73 knockdown in RD cells, a Fusion Negative Rhabdomyosarcoma cell line. We used a Dox-inducible shRNA targetting the 3'UTR of CD73 to knockdown this gene. Cells with No-Dox were used as control.

2024-02-07 | GSE240722 | GEO

CD73 contributes to the pathogenesis of fusion-negative rhabdomyosarcoma through the purinergic signaling pathway.

Project description:Rhabdomyosarcoma (RMS) is the most common type of soft tissue sarcoma in children and adolescents. Fusion-negative RMS (FN-RMS) accounts for more than 80% of all RMS cases. The long-term event-free survival rate for patients with high-grade FN-RMS is below 30%, highlighting the need for improved therapeutic strategies. CD73 is a 5' ectonucleotidase that hydrolyzes AMP to adenosine and regulates the purinergic signaling pathway. We found that CD73 is elevated in FN-RMS tumors that express high levels of TWIST2. While high expression of CD73 contributes to the pathogenesis of multiple cancers, its role in FN-RMS has not been investigated. We found that CD73 knockdown decreased FN-RMS cell growth while up-regulating the myogenic differentiation program. Moreover, mutation of the catalytic residues of CD73 rendered the protein enzymatically inactive and abolished its ability to stimulate FN-RMS growth. Overexpression of wildtype CD73, but not the catalytically inactive mutant, in CD73 knockdown FN-RMS cells restored their growth capacity. Likewise, treatment with an adenosine receptor A2A-B agonist partially rescued FN-RMS cell proliferation and bypassed the CD73 knockdown defective growth phenotype. These results demonstrate that the catalytic activity of CD73 contributes to the pathogenic growth of FN-RMS through the activation of the purinergic signaling pathway. Therefore, targeting CD73 and the purinergic signaling pathway represents a potential therapeutic approach for FN-RMS patients.

| S-EPMC10823247 | biostudies-literature

Expression Profiling of human Fusion-Positive and Fusion-Negative Rhabdomyosarcoma

Project description:Genome-wide gene expression in 33 fusion-positive and 25 fusion-negative rhabdomyosarcoma cases was studied using GeneChip Human Genome U133 Plus2 (Affymetrix) Fusion-positive versus fusion-negative rhabdomyosarcoma tumors

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Fusion Negative Rhabdomyosarcoma Cell Lines

Project description:Fusion Negative Rhabdomyosarcoma Cell Lines

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Expression Profiling of human Fusion-Positive and Fusion-Negative Rhabdomyosarcoma

Project description:Genome-wide gene expression in 33 fusion-positive and 25 fusion-negative rhabdomyosarcoma cases was studied using GeneChip Human Genome U133 Plus2 (Affymetrix)

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Clinical Application of Prognostic Gene Expression Signature in Fusion Gene-Negative Rhabdomyosarcoma

Project description:To date, there are no known prognostic markers identified in patients with fusion gene-negative rhabdomyosarcoma. This study validates the 5-gene (MG5) signature as a prognostic marker in patients with fusion negative intermediate-risk rhabdomyosarcoma clearly stratifying this otherwise clinically homogenous population of patients into two risk groups based on outcome. In addition, this analysis was performed using nCounter assay on paraffin embedded tissues and the results were concordant to previously published results using frozen tissues in a different patient cohort. Therefore, this work holds tremendous translational relevance as the MG5 signature can be reliably assessed in readily available paraffin embedded tissues of fusion gene-negative rhabdomyosarcoma patients in prospective clinical trials to stratify them into prognostic risk groups as well as to potentially tailor future therapy based on these risk groups.

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Defining the interactome of CHD4 in fusion-positive rhabdomyosarcoma

Project description:The goal of this study was to explore in detail how the chromatin remodeler and NuRD subunit CHD4 controls the oncogenic signature of the tumor driver and fusion protein PAX3-FOXO1 in fusion-positive rhabdomyosarcoma. To this aim, we defined the interactome of CHD4 by LC-MS, identified its location in the genome by ChIP-seq, assessed its influence on DNA accessibility by DNase I hypersensitivity assays, and determined its target genes by RNA-seq.

2020-08-11 | PXD015231 | Pride

Gene Expression Profiling of Fusion Negative Rhabdomyosarcoma Cell Lines

Project description:We analyzed the expression of two fusion-negative established Rhabdomyosarcoma cell lines. Together with Chip-seq, we were able to identify transcribed loci bound by myogenic regulatory transcription factors (MYF5 and MYOD) that pertain to embryonic muscle development and cell cycle regulation pathways. Keywords: rhabdomyosarcoma, gene expression profiling, RD, Rh18

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