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

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

PROVIDER: PRJEB67746 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR12145039_1.fastq.gz	Fastqsanger.gz
	ERR12145039_2.fastq.gz	Fastqsanger.gz
	ERR12145040_1.fastq.gz	Fastqsanger.gz
	ERR12145040_2.fastq.gz	Fastqsanger.gz
	ERR12145041_1.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.

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

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

| PRJEB67748 | ENA

Enhancer-associated LncRNA-ITGA2 promotes vascular smooth muscle remodeling by mediating ITGA2 promoter-enhancer interactions

Project description:In this study, multiomics profiling, including CUT&Tag, promoter capture Hi-C (PCHi-C), and microarray, identified LncRNA-ITGA2 as a novel elncRNA that was highly expressed in PDGF-induced proliferative human VSMCs. Notably, LncRNA-ITGA2 was significantly increased in both plasma and coronary atherosclerotic tissues of patients with coronary artery disease (CAD) compared with control subjects. Loss- and gain-of-function studies revealed that LncRNA-ITGA2 potently increased PDGF-induced VSMC proliferation and migration. Moreover, LncRNA-ITGA2 overexpression enhanced neointimal hyperplasia in vivo in a mouse carotid artery injury model, exhibiting its partial functional conservation. RNA-sequencing and CRISPR-Cas9 gene-editing technology revealed integrin α2 (ITGA2) as a downstream target of LncRNA-ITGA2 in VSMCs. Mechanistically, promoter-enhancer interactions were detected by PCHi-C at the ITGA2 locus after PDGF-BB treatment. Chromatin immunoprecipitation sequencing (ChIP-Seq) and chromatin isolation by RNA purification (ChIRP)-qPCR showed that LncRNA-ITGA2 directly bound to the Enhancer-ITGA2 and increased H3K27 acetylation in both the Enhancer-ITGA2 and Promoter-ITGA2. In addition, we demonstrated, by ChIRP-MS and RNA immunoprecipitation, that LncRNA-ITGA2 interacted with the DNA binding-protein NONO (non-pou domain containing octamer-binding protein), which also bound to the ITGA2 promoter, as verified by the ChIP-qPCR assay. Ultimately, the knockout cell lines of NONO, LncRNA-ITGA2, and its promoter confirmed the above regulatory mechanism.

2024-12-31 | GSE248192 | GEO

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.

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Comparison of ITGA2+ trophoblast progenitors to VCT and EVT

Project description:During pregnancy, trophoblast cells in the placenta are the only fetal cells in direct contact with the maternal blood and decidua. They have many functions, including transport of nutrients and oxygen, remodelling the uterine arteries, and communicating with maternal cells. Despite their importance in development and in the success of pregnancy, little is known about human trophoblast progenitors and their differentiation. We identify a proliferative trophoblast niche at the base of cytotrophoblast cell columns in first trimester placentas that is characterised by integrin α2 (ITGA2) expression. Pulse-chase experiments with 5-Iodo-2′-deoxyuridine (IdU) imply that these cells can contribute to both villous and extravillous lineages. Importantly, these cells can be isolated by ITGA2 using flow cytometry and express genes from both VCT and EVT. Microarray shows that they display a unique gene signature including NOTCH signalling and mesenchymal characteristics. ITGA2 allows for the first time the study of a pure population of trophoblast progenitor cells.

2018-03-18 | GSE106852 | GEO

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

2022-02-17 | GSE196732 | GEO

Tead1 regulation of β-cells

Project description:Purpose: The goal of this study is to determine the regulatory role of tead1 in β-cells by analyzing the transcriptomal changes with Tead1 deletion in β-cells Methods: Isolated islet mRNA profiles of β-cell Tead1 KO mice compared to control floxed mice at 1 year of age were assessed by RNA-seq using Illumina Hiseq2500. The sequence reads that passed quality filters were analyzed at the transcript isoform level using the CLC genomic workbench. qRT-PCR validation was performed using SYBR Green assays Conclusions: Our study represents the first detailed analysis of beta cell transcriptomes following Tead1 deletion in beta cells.

2022-12-14 | GSE139152 | GEO

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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Enhancer-associated LncRNA-ITGA2 promotes vascular smooth muscle remodeling by mediating ITGA2 promoter-enhancer interactions

Project description:Enhancer-associated LncRNA-ITGA2 promotes vascular smooth muscle remodeling by mediating ITGA2 promoter-enhancer interactions

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