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IRF4 genome wide binding and transciptomic profile in 501Mel melanoma cell line

ABSTRACT: IRF4 genome wide binding and transciptomic profile in 501Mel melanoma cell line

PROVIDER: PRJNA705651 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13811831_1.fastq.gz	Fastqsanger.gz
	SRR13811831_2.fastq.gz	Fastqsanger.gz
	SRR13811832_1.fastq.gz	Fastqsanger.gz
	SRR13811832_2.fastq.gz	Fastqsanger.gz
	SRR13811833_1.fastq.gz	Fastqsanger.gz

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IRF4 genome wide binding and transciptomic profile in 501Mel melanoma cell line

Project description:To map genome wide binding sites of IRF4, we performed ChIP-seq against eGFP tagged IRF4 in human melanoma cells. To assess whether IRF4 binding influences its target gene expression, RNA-seq was performed after siRNA mediated depletion of IRF4 in 501Mel cells. Subsequently, target genes of IRF4 obtained from ChIP-seq and RNA-seq studies were used to interrogate melanocyte meQTL and identified 131 candidate downstream target CpGs of IRF4, which were validated by cis-/trans-meQTL mediation analysis, suggesting transcription factor mediated expression changes reflected in methylation changes.

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Project description:The proteomes and the miRNomes of melanoma cells and secreted vesicles of normoxic and hypoxic A375, 501Mel, MelJuso and IPC298 melanoma cells were characterized. Here are the data related to the miRNome of cell extracts for the 4 cell lines, in normoxia and hypoxia conditions.

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Project description:Malignant melanoma is an aggressive cancer known for its notorious resistance to most current therapies. The basic helix-loop-helix microphthalmia transcription factor (MITF) is the master regulator determining the identity and properties of the melanocyte lineage, and is regarded as a lineage-specific ‘oncogene’ that has a critical role in the pathogenesis of melanoma. MITF promotes melanoma cell proliferation, whereas sustained supression of MITF expression leads to senescence. By combining chromatin immunoprecipitation coupled to high throughput sequencing (ChIP-seq) and RNA sequen- cing analyses, we show that MITF directly regulates a set of genes required for DNA replication, repair and mitosis. Our results reveal how loss of MITF regulates mitotic fidelity, and through defective replication and repair induces DNA damage, ultimately ending in cellular senescence. These findings reveal a lineage-specific control of DNA replication and mitosis by MITF, providing new avenues for therapeutic intervention in melanoma. The identification of MITF-binding sites and gene- regulatory networks establish a framework for under- standing oncogenic basic helix-loop-helix factors such as N-myc or TFE3 in other cancers. 4 samples corresponding to genomic occupancy profiling of MITF (Cl8), PolII (501Mel), H3K4me3 501Mel). Anti-HA ChIP-seq on untagged cell line (501Mel) was used as a control.

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