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β-catenin programs a tissue-specific epigenetic vulnerability in aggressive adrenocortical carcinoma

ABSTRACT: β-catenin programs a tissue-specific epigenetic vulnerability in aggressive adrenocortical carcinoma

PROVIDER: PRJNA844312 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19503702.fastq.gz	Fastqsanger.gz
	SRR19503703.fastq.gz	Fastqsanger.gz
	SRR19503704.fastq.gz	Fastqsanger.gz
	SRR19503705.fastq.gz	Fastqsanger.gz
	SRR19503706.fastq.gz	Fastqsanger.gz

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Project description:Adrenocortical carcinoma (ACC) is a rare cancer in which tissue-specific differentiation is paradoxically associated with dismal outcomes. The differentiated ACC subtype CIMP-high is prevalent, incurable, and routinely fatal. CIMP-high ACC possess abnormal DNA methylation and frequent β-catenin activating mutations. Here, we demonstrate that this differentiated state is maintained by a balance between nuclear, tissue-specific β-catenin-containing complexes and the ACC epigenome. On chromatin, β-catenin binds master adrenal transcription factor SF1 and hijacks the adrenocortical super-enhancer landscape to maintain differentiation. Off chromatin, β-catenin binds histone methyltransferase EZH2, which is redistributed by the CIMP-high DNA methylation signature. SF1/β-catenin and EZH2/β-catenin complexes exist in normal adrenals and are selected for through all phases of ACC evolution. EZH2 inhibition in CIMP-high ACC favors EZH2/β-catenin assembly and purges SF1/β-catenin from chromatin, erasing differentiation and restraining cancer growth in vitro and in vivo. Our studies illustrate how tissue-specific programs shape oncogene selection, surreptitiously encoding targetable therapeutic vulnerabilities.

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β-catenin programs a tissue-specific epigenetic vulnerability in aggressive adrenocortical carcinoma

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