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SP1 undergoes phase separation and activates RGS20 expression through super-enhancers to promote lung adenocarcinoma progression (CUT＆RUN)

ABSTRACT: SP1 undergoes phase separation and activates RGS20 expression through super-enhancers to promote lung adenocarcinoma progression (CUT＆RUN)

PROVIDER: PRJNA1124850 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29430802_1.fastq.gz	Fastqsanger.gz
	SRR29430802_2.fastq.gz	Fastqsanger.gz
	SRR29430803_1.fastq.gz	Fastqsanger.gz
	SRR29430803_2.fastq.gz	Fastqsanger.gz
	SRR29430804_1.fastq.gz	Fastqsanger.gz

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SP1 undergoes phase separation and activates RGS20 expression through super-enhancers to promote lung adenocarcinoma progression (CUT＆RUN)

Project description:Lung adenocarcinoma (LUAD) is the leading cause of cancer-related death worldwide, but the underlying molecular mechanisms remain largely unclear. The transcription factor SP1 plays a crucial role in the development of various cancers, including LUAD. Recent studies have indicated that master transcription factors may form phase-separated macromolecular condensates to promote super-enhancer assembly and oncogene expression. In this study, we demonstrated that SP1 undergoes phase separation and that its zinc finger 3 in the DNA binding domain is essential for this process. Through CUT&RUN using antibodies against SP1 and H3K27ac, we discovered a significant correlation between SP1 enrichment and super-enhancer elements, identified the regulator of G protein signaling 20 (RGS20) gene as the most likely target regulated by SP1 through super-enhancer mechanisms, and verified this finding using different approaches. The oncogenic activity of SP1 relies on its phase separation ability and RGS20 gene activation, which can be abolished by GSK-J4, a demethylase inhibitor. Together, our findings provide the first evidence that SP1 regulates its target oncogene expression through phase separation and super-enhancer mechanisms, thereby promoting LUAD cell progression. This study also revealed a novel target for LUAD therapies through intervening in SP1-mediated super-enhancer formation.

2024-06-20 | GSE270008 | GEO

TRL-1 undergoes phase separation to regulate the reproduction and longevity tradeoff

Project description:TRL-1 undergoes phase separation to regulate the reproduction and longevity tradeoff

| PRJNA763584 | ENA

TRL-1 undergoes phase separation to regulate the reproduction and longevity tradeoff

Project description:The antagonistic pleiotropy theory of aging proposes that genes enhancing fitness in early life limit lifespan, but the molecular evidence remains underexplored. By profiling translatome changes in Caenorhabditis elegans during starvation recovery, we demonstrate that an open reading frame (ORF) trl-1 'hidden' within an annotated pseudogene significantly translates upon refeeding. trl-1 mutant animals increase brood sizes but shorten lifespan and specifically impair the germline deficiency-induced longevity. The loss of trl-1 abnormally upregulates the translation of vitellogenin that produces copious yolk to provision eggs, whereas vitellogenin overexpression is known to reduce lifespan. We show that TRL-1 protein undergoes liquid-liquid phase separation, through which TRL-1 granules recruit vitellogenin mRNA and inhibit its translation. These results indicate that trl-1 functions as an antagonistic pleiotropic gene to regulate the reproduction-longevity tradeoff by optimizing nutrient production for the next generation.

2022-03-22 | GSE184209 | GEO

Mithramycin Depletes Sp1 and Activates p53 to Mediate Senescence and Apoptosis of Pleural Mesothelioma Cells

Project description:We used microarrays to detail the global gene expression of mithramycin treated cells, xenografts and sp1 depleted cells with p53 overexpression. MPM cells and xenografts were treated with mithramycin or SP1 depleted/p53 overexpressed MPM cells were selected for RNA extraction and hybridization on Affymetrix microarrays. We sought to see the invitro and invivo effect of mithramycin (pharmacological model) and depletion of SP1 and overexpression of p53 (genetic model).

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Coactivator condensation at super-enhancers links phase separation and gene control

Project description:Coactivator condensation at super-enhancers links phase separation and gene control

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Enhanced Phase Separation Mediated Oncogenicity [HiC]

Project description:Chromosome translocation is known to generate oncogenes such as SS18-SSX1, but the underlying mechanism remains unknown. Here we show that enhanced phase separation acquired by translocation mediates oncogenic transformation. SSX fusion dramatically enhances the phase separation property of SS18 protein through H2AK119ub. Super condensates generated by SS18-SSX recruit acetyltransferases CBP/P300 as wild type SS18, but exclude HDACs such that H3K27ac accumulates abnormally at loci from those normally occupied by SS18, resulting aberrant silencing and activation of target genes. Consistently, we show that inhibition of H3K27ac can attenuate the tumorigenicity of the fusion oncoprotein. These results provide the first case for phase separation as a transforming event to generate oncogene and super phase separation can be targeted for cancer therapy.

2024-05-24 | GSE240467 | GEO

RNA-seq to investigate the phase separation-dependent FUS RNA interactome

Project description:The protein Fused in Sarcoma undergoes liquid-liquid phase separation. To investigate whether this phase transition alters the RNA interactome we purified phase-separated FUS droplets and soluble FUS from HEK 293T cells transfected with GFP-tagged WT FUS or P525L FUS. Phase separated FUS was purified by fluorescence-activated particle sorting (droplets) and soluble FUS by co-Immunoprecipitation (IP) respectively followed by isolation of co-purified RNA. Here we show that phase separation affects the RNA interactome of FUS.

2021-06-23 | E-MTAB-8456 | biostudies-arrayexpress

Enhanced Phase Separation Mediated Oncogenicity [RNA-Seq]

Project description:Chromosome translocation is known to generate oncogenes such as SS18-SSX1, but the underlying mechanism remains unknown. Here we show that enhanced phase separation acquired by translocation mediates oncogenic transformation. SSX fusion dramatically enhances the phase separation property of SS18 protein through H2AK119ub. Super condensates generated by SS18-SSX recruit acetyltransferases CBP/P300 as wild type SS18, but exclude HDACs such that H3K27ac accumulates abnormally at loci from those normally occupied by SS18, resulting aberrant silencing and activation of target genes. Consistently, we show that inhibition of H3K27ac can attenuate the tumorigenicity of the fusion oncoprotein (we do not have the data in your figures?). These results provide the first case for phase separation as a transforming event to generate oncogene and super phase separation can be targeted for cancer therapy.

2024-05-24 | GSE211455 | GEO

Enhanced Phase Separation Mediated Oncogenicity [ChIP-Seq]

Project description:Chromosome translocation is known to generate oncogenes such as SS18-SSX1, but the underlying mechanism remains unknown. Here we show that enhanced phase separation acquired by translocation mediates oncogenic transformation. SSX fusion dramatically enhances the phase separation property of SS18 protein through H2AK119ub. Super condensates generated by SS18-SSX recruit acetyltransferases CBP/P300 as wild type SS18, but exclude HDACs such that H3K27ac accumulates abnormally at loci from those normally occupied by SS18, resulting aberrant silencing and activation of target genes. Consistently, we show that inhibition of H3K27ac can attenuate the tumorigenicity of the fusion oncoprotein (we do not have the data in your figures?). These results provide the first case for phase separation as a transforming event to generate oncogene and super phase separation can be targeted for cancer therapy.

2024-05-24 | GSE211454 | GEO

Enhanced Phase Separation Mediated Oncogenicity [RNA-Seq, 2]

2024-05-24 | GSE240473 | GEO