Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

TEAD transcriptional inhibition in basal cell carcinoma

ABSTRACT: TEAD transcriptional inhibition in basal cell carcinoma

PROVIDER: PRJNA659502 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12521600_1.fastq.gz	Fastqsanger.gz
	SRR12521600_2.fastq.gz	Fastqsanger.gz
	SRR12521601_1.fastq.gz	Fastqsanger.gz
	SRR12521601_2.fastq.gz	Fastqsanger.gz
	SRR12521602_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

TEAD transcriptional inhibition in basal cell carcinoma

Project description:RNA sequencing (RNAseq) of primary keratinocytes from mouse basal cell carcinoma mice (BCC) transduced with pooled siRNAs targeting YAP1 and TAZ (siYT) or non-targeting control siRNA (siCon), and with TEADi or GFP as control

2021-06-09 | GSE156913 | GEO

TEAD inhibition in SCC9 cells

Project description:TEAD inhibition in SCC9 cells

| PRJNA659499 | ENA

TEAD inhibition in human keratinocytes

Project description:TEAD inhibition in human keratinocytes

| PRJNA563904 | ENA

YAP-TEAD signaling promotes Basal Cell Carcinoma development via c-JUN/AP1 axis

Project description:YAP-TEAD signaling promotes Basal Cell Carcinoma development via c-JUN/AP1 axis

| PRJNA474193 | ENA

Targeting YAP/TAZ-TEAD as a precision therapy approach in head and neck squamous cell carcinoma

Project description:Dysregulation of the Hippo pathway and the consequent activation of its downstream targets, the transcriptional co-activators YAP and TAZ (YAP/TAZ), drives oncogenic transcriptional programs upon binding TEAD transcription factors in multiple human malignancies. The recent development of small molecule TEAD inhibitors (smTEADi) provides an opportunity to therapeutically target Hippo pathway dysregulation in cancer. In this regard, HPV-negative head and neck squamous cell carcinoma (HNSCC) harbor multiple genetic alterations that promote YAP/TAZ hyperactivation, raising the possibility that HNSCC cells might be dependent on YAP/TAZ-TEAD driven oncogenic transcriptional programs. To test this hypothesis, we examined the antitumor activity of the novel smTEADi, SW-682 and genetically encoded TEAD inhibitor peptide (pTEADi) in Cal33 HPV-negative HNSCC cell line-derived xenograft model. To elucidate the transcriptomic changes upon YAP/TAZ-TEAD inhibition, RNA extracted from xenograft tumors treated with SW-682 or pTEADi, as well as control, was subjected to RNA sequencing.

2024-10-01 | GSE277859 | GEO

Investigating transcriptional programs regulating invasion in basal cell carcinoma

Project description:Investigating transcriptional programs regulating invasion in basal cell carcinoma through scRNAseq analysis

2024-05-31 | GSE266665 | GEO

Investigating transcriptional programs regulating invasion in basal cell carcinoma

Project description:Investigating transcriptional programs regulating invasion in basal cell carcinoma

| PRJNA1108231 | ENA

YAP-TEAD signaling promotes Basal Cell Carcinoma development via c-JUN/AP1 axis [RNA-seq]

Project description:YAP-TEAD signaling promotes Basal Cell Carcinoma development via c-JUN/AP1 axis [RNA-seq]

| PRJNA473926 | ENA

YAP-TEAD signaling promotes Basal Cell Carcinoma development via c-JUN/AP1 axis [ChIP-seq]

Project description:YAP-TEAD signaling promotes Basal Cell Carcinoma development via c-JUN/AP1 axis [ChIP-seq]

| PRJNA474194 | 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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data