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PHF19 drives PRC2 sub-nuclear compartmentalization to promote motility in TNBC cells [RNA-seq]

ABSTRACT: PHF19 drives PRC2 sub-nuclear compartmentalization to promote motility in TNBC cells [RNA-seq]

PROVIDER: PRJNA1232645 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32590330_1.fastq.gz	Fastqsanger.gz
	SRR32590330_2.fastq.gz	Fastqsanger.gz
	SRR32590331_1.fastq.gz	Fastqsanger.gz
	SRR32590331_2.fastq.gz	Fastqsanger.gz
	SRR32590332_1.fastq.gz	Fastqsanger.gz

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PHF19 drives PRC2 sub-nuclear compartmentalization to promote motility in TNBC cells [RNA-seq]

Project description:Polycomb Repressive Complex 2 (PRC2), a master regulator of gene expression and chromatin organization, is frequently hijacked in aggressive malignancies such as triple-negative breast cancer (TNBC). Here, we identify a distinct spatial organization of PRC2 in TNBC cells, where the complex assembles into micron-sized nuclear bodies. Using high-resolution spatial proteomics on these endogenous compartments, we identify PHD Finger Protein 19 (PHF19) as the central driver of these structures. We further demonstrate that an intrinsically disordered region (IDR) within PHF19 promotes its clustering into nuclear bodies and link this spatial organization to enhanced cell motility. These findings shed light on a previously unrecognized layer of PRC2 regulation in TNBC cells, demonstrating how its subnuclear compartmentalization, shaped by accessory subunits, orchestrates functional outcomes critical for cancer progression.

2025-03-14 | GSE291243 | GEO

PHF19 drives PRC2 sub-nuclear compartmentalization to promote motility in TNBC cells [ChIP-seq]

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PHF19 drives PRC2 sub-nuclear compartmentalization to promote motility in TNBC cells [ChIP-seq]

Project description:PHF19 drives PRC2 sub-nuclear compartmentalization to promote motility in TNBC cells [ChIP-seq]

| PRJNA1232644 | ENA

PHF19 drives the formation of PRC2 clusters to enhance motility in TNBC cells

Project description:Polycomb Repressive Complex 2 (PRC2) is a key regulator of transcriptional repression and chromatin organization, essential in development and disease. While its enzymatic activity is well characterized, the factors governing PRC2 subnuclear organization, particularly in cancer cells, are largely unknown. Here, we integrate in situ subcellular proteomics, high-resolution imaging, and functional genomics to investigate PRC2 compartmentalization in triple-negative breast cancer (TNBC) cells. We identify PHF19, a sub-stoichiometric PRC2 accessory subunit as upregulated in TNBC, and central to the formation of endogenous, micron-scale nuclear PRC2 clusters. These structures act as spatial hubs that stabilize local PRC2 occupancy and reinforce H3K27me3 macro-domain organization. Mechanistically, an intrinsically disordered region (IDR) in PHF19 is required for clustering and for promoting TNBC cell motility. Our findings uncover a non-enzymatic layer of PRC2 regulation, where local PRC2 compartmentalization through accessory subunits, directly influences cellular behavior, with implications for disease and development.

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Polycomb PHF19 binds H3K36me3 and recruits PRC2 and demethylase NO66 to embryonic stem cell genes during differentiation

Project description:The Polycomb group proteins are repressive chromatin modifiers with essential roles in metazoan development, cellular differentiation and cell fate maintenance. How Polycomb proteins access active chromatin in order to confer transcriptional silencing during lineage transitions remains unclear. Here we show that the Polycomb Repressive Complex 2 (PRC2) component PHF19 binds the active chromatin mark H3K36me3 via its tudor domain. PHF19 associates with the H3K36me3 demethylase NO66, and is required to recruit the PRC2 complex and NO66 to stem cells genes during differentiation, leading to PRC2 mediated H3K27 tri-methylation, loss of H3K36me3 and transcriptional silencing. We propose a model whereby PHF19 functions during ES cell differentiation to transiently bind the H3K36me3 mark via its tudor domain, forming essential contact points that allow recruitment of PRC2 and H3K36me3 demethylase activity to active gene loci during their transition to a Polycomb-repressed state. Examination of PHF19 genome-wide binding in mouse embryonic stem cells

2012-11-17 | E-GEOD-41609 | biostudies-arrayexpress

Phf19 knockdown effect on F9 embryonal carcinoma cells

Project description:PCL family protein Phf19/Pcl3 is one of the accessory components of the PRC2 core complex, and Phf19 is highly expressed in murine ES cells and an ES cell-like embryonic carcinoma cell line, F9 cells. Here we performed microarray analysis of embryonal carcinoma cell line F9 following Phf19 knockdown by shRNA. Knocking down Phf19/Pcl3 in F9 embryonic cells led to derepression of numerous PRC2 direct target genes. 4 sampels including 2 shRNA vector control cell lines and 2 shPhf19 cell lines were used for RNA extraction and Affymetrix mouse 430 2.0 arrays.

2012-12-20 | E-GEOD-42463 | biostudies-arrayexpress

miR-155 enhances PRC2 activity via polycomb-like protein Phf19 to sustain T cell antitumor immunity [RNA-Seq]

Project description:The microRNA miR-155 is essential for CD8+ T cell antiviral and antitumor immunity but the mechanisms behind its activity remain unresolved. Here, we show that miR-155 increased CD8+ T cell antitumor function by restraining T cell senescence and functional exhaustion through epigenetic silencing of key drivers of effector differentiation. miR-155 enhanced the function of polycomb repressor complex 2 (PRC2) indirectly by promoting the expression of the PRC2 cofactor Phf19 via AKT signaling. Phf19 orchestrated a transcriptional program extensively shared with miR-155 to enhance T cell engraftment, polyfunctionality, and antitumor immunity. These effects were dependent on the histone-binding capacity of Phf19 which is critical for the PRC2 recruitment to chromatin. These findings establish miR-155–Phf19–PRC2 as a pivotal axis regulating CD8+ T cell differentiation. Targeting the microRNA–polycomb-group protein circuitry is a promising route to potentiate cancer immunotherapy through epigenetic reprogramming of CD8+ T cell fate.

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miR-155 enhances PRC2 activity via polycomb-like protein Phf19 to sustain T cell antitumor immunity [ChIP-Seq]

2019-03-11 | GSE99918 | GEO

Polycomb PHF19 binds H3K36me3 and recruits PRC2 and demethylase NO66 to embryonic stem cell genes during differentiation

2012-11-17 | GSE41609 | GEO

Phf19 knockdown effect on F9 embryonal carcinoma cells

2012-12-20 | GSE42463 | GEO