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Conditional expression of sh-YAP1 modulates YAP1/TEAD-dependent transcription and causes regression of established human malignant mesothelioma MSTO-211H [sh-YAP1] xenografts.

ABSTRACT: Conditional expression of sh-YAP1 modulates YAP1/TEAD-dependent transcription and causes regression of established human malignant mesothelioma MSTO-211H [sh-YAP1] xenografts.

PROVIDER: PRJNA806795 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18013322.fastq.gz	Fastqsanger.gz
	SRR18013323.fastq.gz	Fastqsanger.gz
	SRR18013324.fastq.gz	Fastqsanger.gz
	SRR18013325.fastq.gz	Fastqsanger.gz
	SRR18013326.fastq.gz	Fastqsanger.gz

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Conditional expression of sh-YAP1 modulates YAP1/TEAD-dependent transcription and causes regression of established human malignant mesothelioma MSTO-211H [sh-YAP1] xenografts.

Project description:We investigate the dependence of human malignant pleural mesothelioma on a functional YAP1-TEAD transcription factor complex to maintain fully established tumors in vivo. We show that, in a dysfunctional Hippo genetic background, downregulation of YAP1 by shRNA results in modulation of YAP1/TEAD-dependent gene expression and regression of established tumor xenografts. Our data demonstrate that, in the context of a mutated Hippo pathway, YAP1 activity is essential to maintain the growth of mesothelioma cells in vivo, thus validating the concept of inhibiting the activated YAP1/TEAD complex for the treatment of malignant pleural mesothelioma patients.

2022-02-17 | GSE196672 | GEO

RNA-seq of malignant pleural mesothelioma cell line MSTO-211H upon silencing of lncRNA linc00941

Project description:Identification of transcriptional program influenced by the expression of lncRNA linc00941 in malignant pleural mesothelioma cell line MSTO-211H. Linc00941 expression was knocked-down through siRNA strategy.

2024-09-30 | E-MTAB-13400 | biostudies-arrayexpress

Pharmacodynamics of malignant mesothelioma MSTO-211H dn-TEAD2 xenograft recurrence.

Project description:We investigate the dependence of human malignant pleural mesothelioma on a functional YAP1-TEAD transcription factor complex to maintain fully established tumors in vivo. We show that, in a dysfunctional Hippo genetic background, expression of a doxycycline-dependent dominant negative TEAD2 temporarily modulates YAP1/TEAD-dependent gene expression and inhibits growth of established tumor xenografts. Recovery of tumor growth is associated with TEAD-dependent transcription comparable to untreated tumors, therefore, re-activation of TEAD transcription complexes.

2022-02-17 | GSE196714 | GEO

Conditional expression of a dominant negative-TEAD2 construct modulates YAP1/TEAD-dependent transcription and arrests growth of human malignant mesothelioma MSTO-211H [TEAD2-dn] xenografts.

Project description:We investigate the dependence of human malignant pleural mesothelioma on a functional YAP1-TEAD transcription factor complex to maintain fully established tumors in vivo. We show that, in a dysfunctional Hippo genetic background, expression of a dominant negative TEAD2 modulates YAP1/TEAD-dependent gene expression and inhibits growth of established tumor xenografts. Our data demonstrate that, in the context of a mutated Hippo pathway, TEAD2 activity is essential to maintain the growth of mesothelioma tumors in vivo, thus validating the concept of inhibiting the activated YAP1/TEAD complex for the treatment of malignant pleural mesothelioma patients.

2022-02-17 | GSE196691 | GEO

Pharmacodynamics of malignant mesothelioma MSTO-211H dn-TEAD2 xenograft recurrence.

Project description:Pharmacodynamics of malignant mesothelioma MSTO-211H dn-TEAD2 xenograft recurrence.

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Conditional expression of a dominant negative-TEAD2 construct modulates YAP1/TEAD-dependent transcription and arrests growth of human malignant mesothelioma MSTO-211H [TEAD2-dn] xenografts.

Project description:Conditional expression of a dominant negative-TEAD2 construct modulates YAP1/TEAD-dependent transcription and arrests growth of human malignant mesothelioma MSTO-211H [TEAD2-dn] xenografts.

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Transcriptomic analysis of MSTO-211H cell variant resistant to CAR T cell therapy

Project description:Transcriptomic analysis of MSTO-211H cell variant resistant to CAR T cell therapy

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RNA-seq of malignant pleural mesothelioma cell line MSTO-211H upon silencing of lncRNA linc00941

Project description:RNA-seq of malignant pleural mesothelioma cell line MSTO-211H upon silencing of lncRNA linc00941

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The Hippo tranducer YAP1 transforms activated satellite cells and is a potent effector of embryonal rhabdomyosarcoma formation

Project description:The Hippo pathway effector YAP1 controls stem cell fate in epithelial tissues, but its role in stem cells of non-epithelial tissues, such as skeletal muscle, is poorly documented. Here we show that sustained YAP1 activity in mouse activated satellite cells in vivo induces rhabdomyosarcoma (RMS) resembling human embryonal RMS (ERMS) with high penetrance and short latency. The transcriptional program of YAP1 in ERMS drives pro-proliferative pathways whilst decreasing MyoD1 and MEF2 pro-differentiation activity to globally maintain the myoblastic phenotype of ERMS. Normalization of YAP1 expression reduced tumor burden and allowed myogenic differentiation of YAP1-driven and RD ERMS xenografts in situ, thereby identifying YAP1 as a potent RMS-causing oncogene and potential target for differentiation therapy. A total of four samples were analyzed. Two ChIP-Seq datasets from RD human cells, containing reads connected to TEAD binding and IgG binding as control/background; two ChIP-Seq datasets from YAP-ERMS mouse cells, containing reads connected to TEAD binding and Input reads as control/background

2014-08-12 | E-GEOD-55186 | biostudies-arrayexpress

YAP1 exerts its transcriptional control via TEAD mediated activation of enhancers

Project description:YAP is the principle effector of the Hippo signaling pathway; a key regulator of tissue homeostasis whose dysregulation is linked to cancer development. YAP regulation of gene expression is thought to involve the TEAD transcription factor family. Here we show that YAP and TEAD1 binding always co-occurs and is mediated by single as well as double TEAD1 motifs with a particular 3bp spacer (CATTCCNNNCATTCC). This suggests that YAP activity appears exclusively mediated by TEAD1. Despite being characterized as a promoter-binding factor YAP/TEAD actually binds predominantly to enhancers. Moreover we show that YAP is necessary for activity of the linked gene and proper chromatin state of regulated enhancers. These results establish mode of binding and activation of YAP mediated nuclear response of the Hippo pathway by TEAD1 and provide a comprehensive list and a novel class of direct target genes that are regulated distally and could be exploited for cancer therapeutics. Sequencing of ChIP and input samples for YAP1 and TEAD1 transcription factors and H3K27ac histone modification in SF268 glioblastoma cells and for YAP1 transcription factor in NCI-H2052 mesothelioma cells.

2015-08-25 | E-GEOD-61852 | biostudies-arrayexpress

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