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Dampened regulatory circuitry of TEAD1/ITGA1/ITGA2 promotes TGFβ1 signaling to orchestrate prostate cancer progression

ABSTRACT: ChIP-seq data for studying TEAD1 in prostate PC3 cells.

PROVIDER: PRJEB67748 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR12145085.fastq.gz	Fastqsanger.gz
	ERR12145086.fastq.gz	Fastqsanger.gz

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Dampened Regulatory Circuitry of TEAD1/ITGA1/ITGA2 Promotes TGFβ1 Signaling to Orchestrate Prostate Cancer Progression.

Project description:The extracellular matrix (ECM) undergoes substantial changes during prostate cancer (PCa) progression, thereby regulating PCa growth and invasion. Herein, a meta-analysis of multiple PCa cohorts is performed which revealed that downregulation or genomic loss of ITGA1 and ITGA2 integrin genes is associated with tumor progression and worse prognosis. Genomic deletion of both ITGA1 and ITGA2 activated epithelial-to-mesenchymal transition (EMT) in benign prostate epithelial cells, thereby enhancing their invasive potential in vitro and converting them into tumorigenic cells in vivo. Mechanistically, EMT is induced by enhanced secretion and autocrine activation of TGFβ1 and nuclear targeting of YAP1. An unbiased genome-wide co-expression analysis of large PCa cohort datasets identified the transcription factor TEAD1 as a key regulator of ITGA1 and ITGA2 expression in PCa cells while TEAD1 loss phenocopied the dual loss of α1- and α2-integrins in vitro and in vivo. Remarkably, clinical data analysis revealed that TEAD1 downregulation or genomic loss is associated with aggressive PCa and together with low ITGA1 and ITGA2 expression synergistically impacted PCa prognosis and progression. This study thus demonstrated that loss of α1- and α2-integrins, either via deletion/inactivation of the ITGA1/ITGA2 locus or via loss of TEAD1, contributes to PCa progression by inducing TGFβ1-driven EMT.

| S-EPMC10953553 | biostudies-literature

Dampened regulatory circuitry of TEAD1/ITGA1/ITGA2 promotes TGFβ1 signaling to orchestrate prostate cancer progression

Project description:RNA-seq of ITGA1, ITGA2, or TEAD1 knockout in prostate RWPE1/PC3 cells.

| PRJEB67746 | ENA

Dampened regulatory circuitry of TEAD1/ITGA1/ITGA2 promotes TGFβ1 signaling to orchestrate prostate cancer progression

Project description:RNA-seq of ITGA1, ITGA2, and TEAD1 knockout in prostate cell lines

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TEAD1 condensates are transcriptionally inactive storage sites on the pericentromeric heterochromatin

Project description:TEA domain transcription factor 1 (TEAD1), a Hippo pathway transcription factor important in cellular homeostasis and development, is increasingly implicated in cancer biology. Here, we reveal a novel role for TEAD1 in organizing nuclear condensates, independent of active transcription. Using high-resolution imaging, ChIP-seq, RNA-seq and proximity-based proteomics, we demonstrate that in patient-derived renal cell carcinoma cells, TEAD1 forms micron-sized foci by binding to the heterochromatic pericentromeric regions using its DNA-binding domain. These TEAD1 foci do not mediate transcription but instead serve as depots for excess TEAD1. This contrasts with TEAD1 organization in other genomic regions of both RCC and normal kidney cells, where TEAD1 associates with markers of active transcription. Our findings provide a mechanistic framework for TEAD1’s dual regulatory roles, offering new insights into its contribution to transcriptional dysregulation and tumor progression.

2025-06-02 | PXD064255 | Pride

ChIP-Seq in MSK-PCa3 Prostate Cancer Organoids of FOSL1, TAZ, TEAD1, YAP

Project description:Genome-wide mapping of FOSL1, YAP, TAZ and TEAD1 binding sites in MSK-PCa3 cells

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Tead1 regulation of β-cells

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New targets of TEAD1 revealed by ChIP-on-chip

Project description:TEAD1 acts as a key molecule of muscle development, and trans-activates multiple target genes involved in cell proliferation and differentiation pathways. However, its target genes in skeletal muscles, regulatory mechanisms and networks are unknown. Here, we use ChIP-on-chip to identify direct target genes of TEAD1. All animal procedures were performed according to protocols approved by Hubei Province, P. R. China for Biological Studies Animal Care and Use Committee. Skeletal muscle tissues were collected from three adult Kunming mice.

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Tead1 is required to maintain adult cardiomyocyte function

Project description:Since Tead1 binds to MCAT promoter elements to regulate many muscle-specific genes, we performed a global transcriptome analysis in Tead1-deleted adult mouse hearts to assess Tead1 regulated pathways critical to CM function.

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Tead1 regulation of β-cells II

Project description:Purpose: The goal of this study is to determine the regulatory role of Tead1 in β-cells by analyzing the Tead1 cistrome and open chromatin in β-cells Methods: Isolated islets from WT C57bl6 mice of 12 weeks of age were flash frozen. For Chip-seq they were fixed with formaldehyde and then after sonication, IP was performed with Anti-Tead1 antibody or the IgG isotype control. For ATAC-seq 100,000 of the frozen nuclei were tagmented. After DNA extraction, library construction, sequencing was performed using Illumina Hi seq2500. Conclusions: Our study represents the first detailed analysis of the Tead1 cistrome in beta cells.

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Expression data from Tead1 beta cell KO

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