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Loss of Polycomb Repressive Complex 1 activity and chromosomal instability drive uveal melanoma progression

ABSTRACT: Loss of Polycomb Repressive Complex 1 activity and chromosomal instability drive uveal melanoma progression

PROVIDER: PRJNA674769 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12990873_1.fastq.gz	Fastqsanger.gz
	SRR12990873_2.fastq.gz	Fastqsanger.gz
	SRR12990890_1.fastq.gz	Fastqsanger.gz
	SRR12990890_2.fastq.gz	Fastqsanger.gz
	SRR12990891_1.fastq.gz	Fastqsanger.gz

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Loss of Polycomb Repressive Complex 1 activity and chromosomal instability drive uveal melanoma progression

Project description:Chromosomal instability (CIN) and epigenetic alterations have been implicated in tumor progression and metastasis. Yet, how these two hallmarks of cancer are related remains poorly understood. By integrating genetic, epigenetic, and functional analyses at the single cell level, we show that the progression of uveal melanoma (UM), the most common intraocular primary cancer, is driven by loss of Polycomb Repressive Complex 1 (PRC1) in a subpopulation of tumor cells. This is done by transcriptionally profiling 17,074 single cells obtained from fresh surgical human samples taken from primary tumors (n = 6). These samples were derived from patients spanning various stages of tumour progression without enrichment for a specific cell type, such that the entire tumour and its microenvironment were sampled in an unbiased manner. Data from all patients were merged to create a global cell atlas.

2021-08-05 | GSE160883 | GEO

Loss of polycomb repressive complex 1 activity and chromosomal instability drive uveal melanoma progression.

Project description:Chromosomal instability (CIN) and epigenetic alterations have been implicated in tumor progression and metastasis; yet how these two hallmarks of cancer are related remains poorly understood. By integrating genetic, epigenetic, and functional analyses at the single cell level, we show that progression of uveal melanoma (UM), the most common intraocular primary cancer in adults, is driven by loss of Polycomb Repressive Complex 1 (PRC1) in a subpopulation of tumor cells. This leads to transcriptional de-repression of PRC1-target genes and mitotic chromosome segregation errors. Ensuing CIN leads to the formation of rupture-prone micronuclei, exposing genomic double-stranded DNA (dsDNA) to the cytosol. This provokes tumor cell-intrinsic inflammatory signaling, mediated by aberrant activation of the cGAS-STING pathway. PRC1 inhibition promotes nuclear enlargement, induces a transcriptional response that is associated with significantly worse patient survival and clinical outcomes, and enhances migration that is rescued upon pharmacologic inhibition of CIN or STING. Thus, deregulation of PRC1 can promote tumor progression by inducing CIN and represents an opportunity for early therapeutic intervention.

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PRAME induces genomic instability in uveal melanoma

Project description:PRAME induces genomic instability in uveal melanoma

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PRAME induces genomic instability in uveal melanoma [ChIP-Seq]

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Chromosomal changes in primary human uveal melanomas [UCSF]

Project description:Uveal melanoma is the most common cancer of the eye arising from melanocytes within the choroid, ciliary bodies and iris. Almost half of uveal melanomas metastasize hematogenously to distant organs, most often the liver, where the disease becomes fatal. One of the first genetic alterations to be identified in primary uveal melanomas was monosomy 3, which was found to be strongly associated with metastasis. We used gene expression profiling to identify two phenotypically distinct classes of uveal melanomas: class 1 tumors with low-grade morphology and low metastatic risk; and class 2 tumors with aggressive morphology and high metastatic risk. Our initial studies suggested that gene expression profiling was a better predictor of metastasis than monosomy 3. For this study, BAC-array comparative genomic hybridization was used to assay genomic DNA isolated from fresh frozen primary uveal melanoma samples of known molecular class based on gene expression profiling. Independent samples were sent to the aCGH cores at the University of California, San Francisco and the Roswell Park Cancer Institute for hybridization, and log2 ratios were reported. Total genomic DNA was obtained from tumor samples that were collected at the time of treatment. Samples were analyzed by the Microarray Shared Resource at the Comprehensive Cancer Center, University of California, San Francisco or by the Microarray and Genomics Facility of the Roswell Park Cancer Institute.

2012-12-06 | E-GEOD-42739 | biostudies-arrayexpress

Chromosomal changes in primary human uveal melanomas [RPCI]

2012-12-06 | E-GEOD-42738 | biostudies-arrayexpress

Direct Recruitment of Polycomb Repressive Complex 1 (PRC1) to Chromatin by Core Binding Transcription Factors

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