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USP44 overexpression drives a MYC-like gene expression program in neuroblastoma through epigenetic reprogramming

ABSTRACT: USP44 overexpression drives a MYC-like gene expression program in neuroblastoma through epigenetic reprogramming

PROVIDER: PRJNA948371 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23956700_1.fastq.gz	Fastqsanger.gz
	SRR23956700_2.fastq.gz	Fastqsanger.gz
	SRR23956701_1.fastq.gz	Fastqsanger.gz
	SRR23956701_2.fastq.gz	Fastqsanger.gz
	SRR23956702_1.fastq.gz	Fastqsanger.gz

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USP44 overexpression drives a MYC-like gene expression program in neuroblastoma through epigenetic reprogramming

Project description:USP44 overexpression drives a MYC-like gene expression program in neuroblastoma through epigenetic reprogramming

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USP44 overexpression drives a MYC-like gene expression program in neuroblastoma through epigenetic reprogramming

Project description:USP44 overexpression drives a MYC-like gene expression program in neuroblastoma through epigenetic reprogramming

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USP44 overexpression drives a MYC-like gene expression program in neuroblastoma through epigenetic reprogramming

Project description:USP44 overexpression drives a MYC-like gene expression program in neuroblastoma through epigenetic reprogramming

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USP44 overexpression drives a MYC-like gene expression program in neuroblastoma through epigenetic reprogramming

Project description:Neuroblastoma is an embryonic cancer that disproportionately contributes to death in young children. Sequencing data have uncovered few recurrently mutated genes in this cancer though epigenetic pathways have been implicated in disease pathogenesis. We performed a computational screen of deubiquitinating enzymes to identify potential new targets and identified the histone H2B deubiquitinating enzyme USP44 as significantly over-expressed in high-risk tumors. High levels of USP44 significantly correlate with metastatic disease, unfavorable histology, advanced patient age, and MYCN-amplification. The subset of patients with tumors expressing high levels of USP44 have a significantly worse survival, including those with tumors lacking MYCN-amplification. Depleting USP44 in neuroblastoma cell lines leads to diminished proliferation, migration, invasion, as well as impaired neuritic development in response to retinoic acid. Integrated analysis of RNA-seq and ChIP-seq demonstrates a distinct set of genes that is regulated by USP44, including those in Hallmark pathways critical to tumorigenesis – findings that were completely reversed by the re-introduction of USP44. We conclude that USP44 is a novel epigenetic regulator that restrains differentiation and promotes aggressive features. Our data further suggests that USP44 may be a novel target in this disease.

2024-06-11 | GSE228130 | GEO

USP44 overexpression drives a MYC-like gene expression program in neuroblastoma through epigenetic reprogramming

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USP44 overexpression drives a MYC-like gene expression program in neuroblastoma through epigenetic reprogramming

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c-MYC drives neuroblastoma tumorigenesis and retinoic acid resistance in zebrafish [RNA-Seq]

Project description:Neuroblastoma is an often intractable tumor that accounts for 15% of childhood cancer deaths. In addition to MYCN amplification in 20% of tumors, 11% express high levels of c-MYC (MYC) protein. To study this newly defined subgroup, we have created a novel transgenic zebrafish model in which overexpression of MYC in the peripheral sympathetic nervous system drives early-onset neuroblastoma.

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c-MYC drives neuroblastoma tumorigenesis and retinoic acid resistance in zebrafish [ATAC-Seq]

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NeuroD1-USP1-N-Myc axis drives tumor progression in neuroblastoma

Project description:NeuroD1-USP1-N-Myc axis drives tumor progression in neuroblastoma

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USP44 Overexpression Drives a MYC-Like Gene Expression Program in Neuroblastoma through Epigenetic Reprogramming.

Project description:Neuroblastoma is an embryonic cancer that contributes disproportionately to death in young children. Sequencing data have uncovered few recurrently mutated genes in this cancer, although epigenetic pathways have been implicated in disease pathogenesis. We used an expression-based computational screen that examined the impact of deubiquitinating enzymes on patient survival to identify potential new targets. We identified the histone H2B deubiquitinating enzyme USP44 as the enzyme with the greatest impact on survival in patients with neuroblastoma. High levels of USP44 significantly correlate with metastatic disease, unfavorable histology, advanced patient age, and MYCN amplification. The subset of patients with tumors expressing high levels of USP44 had significantly worse survival, including those with tumors lacking MYCN amplification. We showed experimentally that USP44 regulates neuroblastoma cell proliferation, migration, invasion, and neuronal development. Depletion of the histone H2B ubiquitin ligase subunit RNF20 resulted in similar findings, strongly implicating this histone mark as the target of USP44 activity in this disease. Integration of transcriptome and epigenome in analyses demonstrates a distinct set of genes that are regulated by USP44, including those in Hallmark MYC target genes in both murine embryonic fibroblasts and the SH-SY5Y neuroblastoma cell line. We conclude that USP44 is a novel epigenetic regulator that promotes aggressive features and may be a novel target in neuroblastoma. Implications: This study identifies a new genetic marker of aggressive neuroblastoma and identifies the mechanisms by which its overactivity contributes to the pathophysiology of this disease.

| S-EPMC11372370 | biostudies-literature

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