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TEAD inhibition in SCC9 cells

ABSTRACT: TEAD inhibition in SCC9 cells

PROVIDER: PRJNA659499 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12521589_1.fastq.gz	Fastqsanger.gz
	SRR12521589_2.fastq.gz	Fastqsanger.gz
	SRR12521590_1.fastq.gz	Fastqsanger.gz
	SRR12521590_2.fastq.gz	Fastqsanger.gz
	SRR12521591_1.fastq.gz	Fastqsanger.gz

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TEAD inhibition in human keratinocytes

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TEAD inhibition in SCC9 cells

Project description:RNA sequencing (RNAseq) of SCC9 cells transduced with TEAD inhibitor protein (TEADi) or control GFP

2021-07-01 | GSE156912 | GEO

Identification of resistance mechanisms to small-molecule inhibition of YAP/TEAD-regulated transcription [RNA-seq]

Project description:The Hippo tumour suppressor pathway controls transcription by regulating nuclear abundance of YAP and TAZ, which activate transcription with the TEAD1-TEAD4 DNA-binding proteins. Recently, several small-molecule inhibitors of YAP and TEADs have been reported, with some now entering clinical trials for different cancers. Here, we investigated the cellular response to TEAD palmitoylation inhibitors, using genomic and genetic strategies. Genome-wide CRISPR/Cas9 screens revealed that mutations in genes from the Hippo, MAPK and JAK-STAT signaling pathways all modulate the cellular response to TEAD inhibition. Inhibition of TEAD palmitoylation strongly reduced YAP/TEAD target expression, whilst only mildly impacting YAP/TEAD genome binding. Additionally, expression of MAPK pathway genes was induced upon inhibition of TEAD palmitoylation, which coincided with YAP/TEAD redistribution to AP-1 transcription factor binding sites. Consistent with this, combined inhibition of TEAD and the MAPK protein MEK, synergistically blocked proliferation of several mesothelioma and lung cancer cell lines and more potently reduced the growth of patient-derived lung cancers in vivo. Collectively, we reveal mechanisms by which cells can overcome small-molecule inhibition of TEAD palmitoylation and potential strategies to enhance the anti-tumor activity of emerging Hippo pathway targeted therapies.

2024-07-08 | GSE269899 | GEO

TEAD transcriptional inhibition in basal cell carcinoma

Project description:TEAD transcriptional inhibition in basal cell carcinoma

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TEAD inhibitor K-975 enhances KRASG12C inhibitor adagrasib-mediated cancer cell proliferation inhibition via dual cell cycle arrest

Project description:Here we investigate the effect of the dual inhibition, in KRASG12C mutated NSCLC cells, using the KRASG12Ci adagrasib (MRTX849) and the pan-TEAD inhibitor (TEADi) K-975. We show that K-975 enhances adagrasib-induced tumor cell growth inhibition in cancer cells. Mechanistically, we detect a downregulation of MYC and E2F signatures and a downregulation of the G2/M checkpoint regulation, which result in the increase of G1 and the decrease of the G2/M cell cycle phases. These data suggest that the co-inhibition of KRASG12C and YAP1-TEAD leads to a specific switch in the mechanism of cancer cell killing.

2023-05-12 | PXD039726 | JPOST Repository

TEAD inhibition in human keratinocytes

Project description:RNA sequencing (RNAseq) of N/TERT2G keratinocytes transduced with TEAD inhibitor protein (TEADi) or control GFP for 12, 24 and 48 hs

2020-02-24 | GSE136876 | GEO

TEAD and YAP regulate the enhancer network of human embryonic pancreatic progenitors

Project description:The genomic regulatory programs that underlie human organogenesis are poorly understood. Human pancreas development, in particular, has pivotal implications for pancreatic regeneration, cancer, and diabetes. We have now created maps of transcripts, active enhancers, and transcription factor networks in pancreatic multipotent progenitors obtained from human embryos, or derived in vitro from human embryonic stem cells. This revealed that artificial progenitors recapitulate salient transcriptional and epigenomic features of their natural counterparts. Using this resource, we show that TEAD1, a transcription factor controlled by Hippo signaling, is a core component of the combinatorial code of pancreatic progenitor enhancers. TEAD thus activates genes encoding regulators of signaling pathways and stage-specific transcription factors that are essential for normal pancreas development. Accordingly, chemical and genetic perturbations of TEAD and its coactivator YAP inhibited expression of known regulators such as FGFR2 and SOX9, and suppressed the proliferation and expansion of mouse and zebrafish pancreatic progenitors. These findings provide a resource of active enhancers and transcripts in human pancreatic multipotent progenitors, and uncover a central role of TEAD and YAP as signal-responsive regulators of the transcriptional program of early pancreas development.

2015-04-06 | E-MTAB-3061 | biostudies-arrayexpress

ATAC-seq of H226 cells treated with TEAD inhibitor GNE-7883

Project description:ATAC-seq of H226 cells treated with TEAD inhibitor GNE-7884

2023-04-26 | GSE229064 | GEO

Lysine long-chain fatty acylation regulates the TEAD transcription factor

Project description:TEAD transcription factors are responsible for the transcriptional output of Hippo signalling1,2. TEAD activity is primarily regulated by phosphorylation of its coactivators YAP and TAZ3,4. In addition, cysteine palmitoylation has recently been shown to regulate TEAD activity5,6. Here, we report lysine long-chain fatty acylation as a novel posttranslational modification of TEADs. Lysine fatty acylation occurs spontaneously via intramolecular transfer of acyl groups from the proximal acylated cysteine residue. Lysine fatty acylation, like cysteine palmitoylation, contributes to the transcriptional activity of TEADs by enhancing the interaction with YAP and TAZ, but it is more stable than cysteine acylation, suggesting that the lysine fatty-acylated TEAD acts as a “stable active form”. Significantly, lysine fatty acylation of TEAD increased upon Hippo signalling activation, despite a decrease in cysteine acylation. Our results provide new insight into the role of fatty acyl modifications in the regulation of TEAD activity.

2023-03-19 | PXD033939 | Pride

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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