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TRPS1 mutant (R544Q) regulates epithelial to mesenchymal transition

ABSTRACT: TRPS1 was selected as a candidate for further exploring the molecular mechanism of CRC distant metastasis according to single cell seq results. We next performed bulk RNA sequencing to explore the underlying mechanism by which TRPS1 R544Q mutation contributes to CRC metastasis.Comparative gene expression profiling analysis of RNA-seq data for HCT116 (control,TRPS1,R544Q）and SW480 (control,TRPS1,R544Q）

ORGANISM(S): Homo sapiens

PROVIDER: GSE206729 | GEO | 2023/12/15

REPOSITORIES: GEO

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TRPS1 mutant (R544Q) regulates epithelial to mesenchymal transition through binding to ZEB1 promoter region

Project description:TRPS1 was selected as a candidate for further exploring the molecular mechanism of CRC distant metastasis according to single cell seq results. As TRPS1 is a transcriptional factor mainly located in cellular nucleus , we performed Cleavage Under Targets and Tagmentation (CUT&Tag) Sequencing assay on TRPS1-WT and TRPS1-MT cells respectively to explore the whole-genome binding site of TRPS1.

2023-12-15 | GSE206564 | 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

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

Phenotypic plasticity underlies local invasion and distant metastasis in colon cancer (Bulk RNA-Seq)

Project description:Phenotypic plasticity and partial EMT underlie local invasion and distant metastasis in colon cancer. CD44highEpCAMhigh and CD44highEpCAMlow RNAseq profiles of colon cancer cell lines HCT116 and SW480.

2020-07-23 | GSE154927 | GEO

RNA-seq analysis of MCF7 cells with/without silencing TRPS1/HDAC2

Project description:We reported the transcriptional regulation function and mechanism of TRPS1.

2021-05-30 | GSE115126 | GEO

Phenotypic plasticity underlies local invasion and distant metastasis in colon cancer (Single cell RNA-Seq)

Project description:Phenotypic plasticity and partial EMT underlie local invasion and distant metastasis in colon cancer. CD44highEpCAMhigh and CD44highEpCAMlow single cell RNAseq profiles of colon cancer cell lines HCT116 and SW480.

2020-07-23 | GSE154930 | GEO

ChIPseq and RNAseq analysis of T47D cells with/without silencing TRPS1/CHD4

Project description:We reported the transcriptional regulation function and mechanism of TRPS1-CHD4/NuRD.

2018-12-26 | GSE114213 | GEO

Transcriptional targets of Trps1 in vibrissae

2011-12-22 | GSE33766 | GEO

TRPS1 impairs myogenic differentiation in embryonal rhabdomyosarcoma [ChIP-seq]

Project description:We report here the analysis of TRPS1 chromatin binding by ChIP-Seq in embryonal rhabdomyosarcoma RD cells. We use here parental and TRPS1-KO RD cells. RD cells and RD-TRPS1-KO cells were cultured in growth medium and chromatin was prepared. TRPS1 DNA binding in RD cells and RD-TRPS1-KO cells using a selfmade antibody (referenced in Elster et al.) was determined by ChIP-seq.

2023-07-24 | GSE197550 | GEO

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

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