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MyoD-Cre driven alterations in K-Ras and p53 lead to a mouse model with histological and molecular characteristics of human rhabdomyosarcoma

ABSTRACT: MyoD-Cre driven alterations in K-Ras and p53 lead to a mouse model with histological and molecular characteristics of human rhabdomyosarcoma

PROVIDER: PRJNA802585 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17847355_1.fastq.gz	Fastqsanger.gz
	SRR17847355_2.fastq.gz	Fastqsanger.gz
	SRR17847356_1.fastq.gz	Fastqsanger.gz
	SRR17847356_2.fastq.gz	Fastqsanger.gz
	SRR17847357_1.fastq.gz	Fastqsanger.gz

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MyoD-Cre driven alterations in K-Ras and p53 lead to a mouse model with histological and molecular characteristics of human rhabdomyosarcoma [RMS_GEMM_tumors]

Project description:MyoD-Cre driven alterations in K-Ras and p53 lead to a mouse model with histological and molecular characteristics of human rhabdomyosarcoma [RMS_GEMM_tumors]

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MyoD-Cre driven alterations in K-Ras and p53 lead to a mouse model with histological and molecular characteristics of human rhabdomyosarcoma [RMS_GEMM_tumors]

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MyoD-Cre driven alterations in K-Ras and p53 lead to a mouse model with histological and molecular characteristics of human rhabdomyosarcoma

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Liaison between SNAI2 and MYOD enhances oncogenesis and suppresses differentiation in Fusion-Negative Rhabdomyosarcoma

Project description:Rhabdomyosarcoma (RMS) is a pediatric malignancy of mesenchymal origin. Fusion Negative-RMS (FN-RMS) tumors are associated with RAS-pathway activation. RMS tumors express pro-differentiation myogenic transcription factors MYOD and MYOG, yet why they are unable to differentiate is poorly understood. Here we show that SNAI2 is highly expressed in FN-RMS, is regulated by MYOD and blocks myogenic differentiation promoting growth. Molecularly, SNAI2 preferentially binds E-Box-associated enhancer elements and represses expression by dampening enhancer function. SNAI2 inhibits MYOD at a subset of myogenic enhancers associated with terminal differentiation. Functional dissection demonstrates SNAI2 suppresses a MYOG, MEF2 and CDKN1A differentiation program. SNAI2 knockdown transcriptionally mimics a chemical blockade of the mutant RAS signal in FN-RMS, providing new insight connecting the genetic and epigenetic causes of this disease.

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ChIP-seq of Active Histone Mark (H3K27ac) and Myogenic Regulatory Factors (MYF5 and MYOD) in Fusion Negative Rhabdomyosarcoma Cell Lines

Project description:We performed Chip-seq analysis of Myogenic Regulatory Transcription Factors (MYF5 and MYOD) in Fusion Negative Rhabdomyosarcoma cell lines. Endogenous MYF5/H3K27ac Chip-seq was performed in Rh18 cells and MYOD-H3K27ac Chip-seq was performed in RD cells, given that these cell lines express these proteins in a mutually-exclusive manner. Analysis revealed a common subset of enhancer and promoter regions bound by these transcription factors that are enriched for cell cycle regulation and embryonic muscle development pathways. Keywords: rhabdomyiosarcoma, Chip-seq, chromatin, Transcription factos, MYF5, MYOD

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