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TRPS1 is a lineage-specific transcriptional dependency in breast cancer [Seq]

ABSTRACT: TRPS1 is a lineage-specific transcriptional dependency in breast cancer [Seq]

PROVIDER: PRJNA471883 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7179560.fastq.gz	Fastqsanger.gz
	SRR7179570.fastq.gz	Fastqsanger.gz
	SRR7179580.fastq.gz	Fastqsanger.gz
	SRR7179590.fastq.gz	Fastqsanger.gz
	SRR7179600.fastq.gz	Fastqsanger.gz

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TRPS1 is a lineage-specific transcriptional dependency in breast cancer

Project description:TRPS1 is a lineage-specific transcriptional dependency in breast cancer

| PRJNA471878 | ENA

TRPS1 is a lineage-specific transcriptional dependency in breast cancer [Seq]

Project description:We performed an unbiased cell viability-based pooled shRNA screen on 59 cell lines to identify novel epigenetic and transcriptional dependencies of multiple cancer types, including leukemia, neuroblastoma, breast, colorectal, prostate, and rhabdoid tumors. Here, we identified Tricho-Rhino-Phalangeal Syndrome Type I protein (TRPS1) as one of the most significant hits specific for breast cancer cell lines. Downregulation of TRPS1 resulted in cell cycle arrest and apoptosis increase in vitro and impaired tumorigenic capacity in vivo. We characterized TRPS1 genomic targets and protein interactome. We identified GATAD2B as an important partner of TRPS1, uncovering novel epigenetic network crucial for breast cancer cell survival.

2018-10-03 | GSE114597 | GEO

TRPS1 is a lineage-specific transcriptional dependency in breast cancer [methylation array]

Project description:TRPS1 is a lineage-specific transcriptional dependency in breast cancer [methylation array]

| PRJNA471882 | ENA

TRPS1 is a lineage-specific transcriptional dependency in breast cancer [methylation array]

2018-10-03 | GSE114598 | GEO

TRPS1 Is a Lineage-Specific Transcriptional Dependency in Breast Cancer.

Project description:Perturbed epigenomic programs play key roles in tumorigenesis, and chromatin modulators are candidate therapeutic targets in various human cancer types. To define singular and shared dependencies on DNA and histone modifiers and transcription factors in poorly differentiated adult and pediatric cancers, we conducted a targeted shRNA screen across 59 cell lines of 6 cancer types. Here, we describe the TRPS1 transcription factor as a strong breast cancer-specific hit, owing largely to lineage-restricted expression. Knockdown of TRPS1 resulted in perturbed mitosis, apoptosis, and reduced tumor growth. Integrated analysis of TRPS1 transcriptional targets, chromatin binding, and protein interactions revealed that TRPS1 is associated with the NuRD repressor complex. These findings uncover a transcriptional network that is essential for breast cancer cell survival and propagation.

| S-EPMC6366939 | biostudies-literature

Transcriptome profiling of radiation-transformed breast cells after TRPS1 siRNA knockdown.

Project description:TRPS1 was recently identified as a radiation marker in breast cancer. In order to characterise the molecular phenotype that is associated with TRPS1 we knocked out the gene in two radiation-transformed breast cell lines.

2017-10-01 | E-MTAB-6008 | biostudies-arrayexpress

RIME against TRPS1 in breast cancer cell lines

Project description:Identification of TRPS1 interactors in MCF7, T47D and ZR75-1 breast cancer cell lines.

2018-06-12 | PXD009863 | Pride

TRPS1 shapes YAP/TEAD-dependent transcription in breast cancer cells

Project description:Yes-associated protein (YAP), the downstream transducer of the Hippo pathway is a key regulator of organ size, differentiation and tumourigenesis. Yet, the activity of YAP can also be modulated by Hippo-independent functions. To disclose these Hippo-independent regulators, we performed a genome-wide CRISPR screening approach that identified the transcriptional repressor protein Trichorhinophalangeal Syndrome 1 (TRPS1) as a potent repressor of YAP-dependent transactivation. Using RNA-Sequencing and ChIP-Sequencing approaches we show that TRPS1 globally regulates YAP-dependent transcription by binding to a large set of joint genomic sites, mainly enhancers. Mechanistically, TRPS1 represses YAP-dependent enhancers function by recruiting a spectrum of corepressor complexes to joint sites. Consequently, loss of TRPS1 leads to activation of enhancers due to increased H3K27 acetylation and an altered promoter-enhancer interaction landscape. TRPS1 is commonly amplified in breast cancer which is associated decreased YAP activity and leads to a decreased frequency of intratumoural immune cells. Consistently, depletion of TRPS1 in the syngeneic 4T1 tumour model leads to a strongly decreased tumour growth in vivo. Our study uncovers TRPS1 as a new epigenetic regulator of YAP activity and it connects repression of YAP-dependent enhancer function to breast cancer. For project-related queries, please contact bjoern.voneyss@leibniz-fli.de <mailto:bjoern.voneyss@leibniz-fli.de>.

2018-08-09 | PXD009819 | Pride

TRPS1 is a lineage-specific transcriptional dependency in breast cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-10-03 | GSE114600 | GEO

Transcriptional targets of Trps1 in vibrissae

Project description:Mutations in TRPS1 cause trichorhinophalangeal syndrome types I and III, which are characterized by sparse scalp hair in addition to craniofacial and skeletal abnormalities. Trps1 is a vertebrate transcription factor containing nine zinc-finger domains, including a GATA-type zinc finger through which it binds DNA. Mice in which the GATA domain of Trps1 has been deleted (Trps1∆gt/∆gt) have a reduced number of pelage follicles and lack vibrissae follicles postnatally. To identify the transcriptional targets of Trps1 in the developing vibrissa follicle, we performed microarray hybridization analysis comparing expression patterns in the whisker pads of wild-type versus Trps1∆gt/∆gt embryos. We identified a number of transcription factors and Wnt inhibitors among transcripts downregulated in the mutant embryos, and several extracellular matrix proteins there were upregulated in the mutant samples. Whole whisker pads were dissected from E12.5 embryos and total RNA was isolated using the RNeasy Mini Kit (Qiagen). Triplicate RNA samples from three independent embryos of each genotype were amplified and labeled for hybridization to Affymetrix GeneChip MOE430A microarrays using Affymetrix reagents and protocols. The data output was analyzed using GeneSpring GX 10.0 commercial software (Agilent Technologies). P-values were calculated using an unpaired t-test. Expression values with a p-value less than or equal to 0.05 and a fold difference of at least 1.5 relative to wild-type baseline expression levels were considered significant.

2011-12-22 | E-GEOD-33766 | biostudies-arrayexpress

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