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Next Generation Sequencing Quantitative Analysis of TEAD Palmitoylation Inhibitor MGH-CP1 in MDA-MB-231 cells

ABSTRACT: Next Generation Sequencing Quantitative Analysis of TEAD Palmitoylation Inhibitor MGH-CP1 in MDA-MB-231 cells

PROVIDER: PRJNA736975 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14788944_1.fastq.gz	Fastqsanger.gz
	SRR14788944_2.fastq.gz	Fastqsanger.gz
	SRR14788945_1.fastq.gz	Fastqsanger.gz
	SRR14788945_2.fastq.gz	Fastqsanger.gz
	SRR14788946_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Next Generation Sequencing Quantitative Analysis of TEAD Palmitoylation Inhibitor MGH-CP1 in MDA-MB-231 cells

Project description:Purpose: The goal of this study is to understand the signaling pathway alteration inMDA-MB-231cells treated with TEAD autopalmitoylation inhibitor MGH-CP1, and to further validate TEAD inhibitor for specifity in TEAD-YAP interuption. Methods:Breast cancer cell line MDA-MB-231 was chosen to be treated with TEAD palmitoylation inhibitor MGH-CP1 at 10μM for 24 hours. Total RNA was isolated for the analysis. RNA samples were sent to Novogen for library construction, RNA sequencing and raw data process. Conclusions: Our study privides gene expression profiling evidence to validate our TEAD palmitoylation inhibitor MGH-CP1 as specific small molecule to block TEAD transcriptional activity.

2022-09-11 | GSE177052 | GEO

Next Generation Sequencing Quantitative Analysis of TEAD Palmitoylation Inhibitor MGH-CP1 in Breast Cancer Cell Line

Project description:Purpose: The goal of this study is to understand the signaling pathway alteration in cancer cell line treated with TEAD palmitoylation inhibitor MGH-CP1, and to further validate TEAD inhibitor for specifity in TEAD-YAP interuption. Methods:Breast cancer cell line MDA-MB-231 was chosen to be treated with TEAD palmitoylation inhibitor MGH-CP1 at 10μM for 24 hours. Total RNA was isolated for the analysis. RNA samples were sent to Novogen for library construction, RNA sequencing and raw data process. Results: MGH-CP1 specifically blocks TEAD transcriptional activity compared with YAP/TAZ siRNA in MDA-MB-231 cells. Conclusions: Our study privides gene expression profiling evidence to validate our TEAD palmitoylation inhibitor MGH-CP1 as specific small molecule to block TEAD transcriptional activity. We report the application of next generation sequencing technology for high-throughput profiling of TEAD palmitoylation inhibitor MGH-CP1 in breast cancer cells.

2021-05-11 | GSE140396 | GEO

Next Generation Sequencing Quantitative Analysis of TEAD Palmitoylation Inhibitor MGH-CP1 in Breast Cancer Cell Line

Project description:Next Generation Sequencing Quantitative Analysis of TEAD Palmitoylation Inhibitor MGH-CP1 in Breast Cancer Cell Line

| PRJNA589597 | ENA

Raw RNA-seq data of MEF cells treated with MGH-CP1

Project description:Raw RNA-seq data of MEF cells treated with control vehicles (DMSO) and MGH-CP1 (1uM in DMSO)for 2 and 4 days

2022-12-01 | GSE141494 | GEO

Next Generation Sequencing Quantitative Analysis of TEAD Palmitoylation Inhibitor TM2 in NCI-H226 cells

Project description:Purpose: The goal of this study is to understand the signaling pathway alteration in NCI-H226 cells treated with new TEAD autopalmitoylation inhibitor TM2, and to further validate TEAD inhibitor for specifity in TEAD-YAP interuption. Methods: Mesothelioma cell line NCI-H226 was chosen to be treated with TEAD palmitoylation inhibitor TM2 at 1μM for 24 hours. Total RNA was isolated for the analysis. RNA samples were sent to Novogen for library construction, RNA sequencing and raw data process. Conclusions: Our study privides gene expression profiling evidence to validate our TEAD palmitoylation inhibitor TM2 as specific small molecule to block TEAD transcriptional activity in mesothelioma cells.

2024-05-01 | GSE203421 | GEO

TEAD1 ChIP-seq on on MDA-MB-231 and Detroit X1 562 cells

Project description:The Hippo Pathway is a critical signaling network that regulates organ size and cellular proliferation in metazoans. The transcriptional enhanced associate domain (TEAD) family of transcription factors serve as the receptors for the downstream effectors of the Hippo pathway, YAP and TAZ, to upregulate expression of multiple genes involved in proliferation, cell-fate determination, polarity, and survival1. Recent work revealed that TEAD proteins are palmitoylated at a conserved cysteine with the lipid tail extending into the hydrophobic core of the protein2. Mutagenic and covalent modulation of the palmitoylation site disrupts Hippo signaling2,3; however, an understanding of why TEAD proteins require this seemingly essential modification and the therapeutic implications of modulating TEAD palmitoylation has remained elusive. Here we report the identification and optimization of a potent pan-TEAD small molecule that binds the TEAD lipid pocket (LP), blocks palmitoylation, and dysregulates TEAD activity in multiple cancer cell lines. Cellular and biochemical data interrogating the mechanism of action for our compound reveal TEAD palmitoylation to function as a checkpoint that regulates TEAD homeostasis. We show that bypassing this checkpoint with a small molecule increases TEAD protein levels thereby decreasing the ability of YAP/TAZ to activate downstream target gene transcription in a dominant-negative manner. Our study demonstrates a new role for lipidation in protein signaling and establishes the TEAD LP as a bona fide therapeutic site for modulation of the Hippo Pathway.

2020-06-03 | GSE139951 | GEO

Changes in gene expression following MGH-CP1 or dinaciclib treatment.

Project description:Changes in gene expression following MGH-CP1 or dinaciclib treatment.

| PRJNA1130043 | ENA

Raw RNA-seq data of MEF cells treated with MGH-CP1

Project description:Raw RNA-seq data of MEF cells treated with MGH-CP1

| PRJNA593607 | ENA

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

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

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