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Disruption of the MSL complex inhibits tumor maintenance by exacerbating chromosomal instability

ABSTRACT: Disruption of the MSL complex inhibits tumor maintenance by exacerbating chromosomal instability

PROVIDER: PRJNA602514 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10919734.fastq.gz	Fastqsanger.gz
	SRR10919735.fastq.gz	Fastqsanger.gz
	SRR10919736.fastq.gz	Fastqsanger.gz
	SRR10919737.fastq.gz	Fastqsanger.gz
	SRR10919738.fastq.gz	Fastqsanger.gz

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Disruption of the MSL complex inhibits tumor maintenance by exacerbating chromosomal instability

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Disruption of the MSL complex inhibits tumour maintenance by exacerbating chromosomal instability.

Project description:Rewiring of cellular programmes in malignant cells generates cancer-specific vulnerabilities. Here, using an unbiased screening strategy aimed at identifying non-essential genes required by tumour cells to sustain unlimited proliferative capacity, we identify the male-specific lethal (MSL) acetyltransferase complex as a vulnerability of genetically unstable cancers. We find that disruption of the MSL complex and consequent loss of the associated H4K16ac mark do not substantially alter transcriptional programmes but compromise chromosome integrity and promote chromosomal instability (CIN) that progressively exhausts the proliferative potential of cancer cells through a p53-independent mechanism. This effect is dependent on pre-existing genomic instability, and normal cells are insensitive to MSL disruption. Using cell- and patient-derived xenografts from multiple cancer types, we show that excessive CIN induced by MSL disruption inhibits tumour maintenance. Our findings suggest that targeting MSL may be a valuable means to increase CIN beyond the level tolerated by cancer cells without inducing severe adverse effects in normal tissues.

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Project description:modENCODE_submission_3293 This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: We aim to determine the locations of 125 chromosomal proteins across the Drosophila melanogaster genome. The proteins under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Cell Line: S2-DRSC; Tissue: embryo-derived cell-line; Developmental Stage: late embryonic stage; Sex: Male; NUMBER OF REPLICATES: 4; EXPERIMENTAL FACTORS: Cell Line S2-DRSC; Antibody MSL-1(Q4453) (target is MSL-1)

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