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YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation

ABSTRACT: YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation

PROVIDER: PRJNA702446 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13731713.fastq.gz	Fastqsanger.gz
	SRR13731714.fastq.gz	Fastqsanger.gz
	SRR13731715.fastq.gz	Fastqsanger.gz
	SRR13731716.fastq.gz	Fastqsanger.gz
	SRR13731717.fastq.gz	Fastqsanger.gz

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YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation (RNA-seq)

Project description:The YAP and TAZ paralogues, the ultimate effectors of the Hippo signaling pathway, are deregulated in many cancer types. They are transcriptional co-activators that are recruited to their target sites, primarily by TEAD proteins. Here, we show that YAP and TAZ are also recruited by JUNB and STAT3, key factors that mediate an epigenetic switch linking inflammation to breast cellular transformation. YAP and TAZ directly interact with JUNB and STAT3 via a WW domain that is important for transformation, co-occupy many target sites in vivo via the sequence motifs of AP-1 and (to a lesser extent) STAT3, and stimulate transcriptional activation by AP-1 proteins. A small minority of target sites are YAP- or TAZ-specific, and they are associated with different sequence motifs and gene classes. YAP/TAZ, JUNB, and STAT3 directly regulate a common set of target genes that overlap, but are distinct from, those regulated by YAP/TAZ and TEADs. The set of target genes regulated by YAP/TAZ, STAT3, and JUNB is associated with poor survival in breast cancer patients with the triple-negative form of the disease.

2021-02-18 | GSE166942 | GEO

YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation (ChIP-seq)

2021-02-18 | GSE166941 | GEO

YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation (ChIP-seq)

Project description:YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation (ChIP-seq)

| PRJNA702452 | ENA

YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation (RNA-seq)

Project description:YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation (RNA-seq)

| PRJNA702453 | ENA

YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation.

Project description:The YAP and TAZ paralogs are transcriptional co-activators recruited to target sites by TEAD proteins. Here, we show that YAP and TAZ are also recruited by JUNB (a member of the AP-1 family) and STAT3, key transcription factors that mediate an epigenetic switch linking inflammation to cellular transformation. YAP and TAZ directly interact with JUNB and STAT3 via a WW domain important for transformation, and they stimulate transcriptional activation by AP-1 proteins. JUNB, STAT3, and TEAD co-localize at virtually all YAP/TAZ target sites, yet many target sites only contain individual AP-1, TEAD, or STAT3 motifs. This observation and differences in relative crosslinking efficiencies of JUNB, TEAD, and STAT3 at YAP/TAZ target sites suggest that YAP/TAZ is recruited by different forms of an AP-1/STAT3/TEAD complex depending on the recruiting motif. The different classes of YAP/TAZ target sites are associated with largely non-overlapping genes with distinct functions. A small minority of target sites are YAP- or TAZ-specific, and they are associated with different sequence motifs and gene classes from shared YAP/TAZ target sites. Genes containing either the AP-1 or TEAD class of YAP/TAZ sites are associated with poor survival of breast cancer patients with the triple-negative form of the disease.

| S-EPMC8463077 | biostudies-literature

YAP/TAZ cooperate with AP-1 to drive the mesenchymal cell state in neuroblastoma [ATACseq]

Project description:Cellular plasticity is a major driver of therapy resistance in cancer. For the pediatric solid tumor neuroblastoma, two distinct tumor cell phenotypes have been identified: adrenergic (ADR) and mesenchymal (MES) cells. Of those, the MES cells pose a rare subtype resistant to common treatment options. Here, we developed an image-based compound screen to interrogate vulnerabilities specific to the MES phenotype at single-cell resolution in heterogeneous neuroblastoma cultures. Among the top hits, we identified inhibition of the transcriptional co-activators YAP/TAZ as a specific target in MES cells. Based on their chromatin binding, we show that YAP/TAZ cooperate with AP-1 transcription factors to regulate MES gene expression by forming a core-regulatory circuitry. We further provide evidence of a subset of tumor cells in patients co-expressing these factors. Collectively, we demonstrate that YAP/TAZ and AP-1 drive neuroblastoma tumor cell plasticity and present a novel therapeutic vulnerability with the potential to overcome treatment resistance.

2025-10-02 | GSE275985 | GEO

YAP/TAZ cooperate with AP-1 to drive the mesenchymal cell state in neuroblastoma [RNAseq]

2025-10-02 | GSE275995 | GEO

YAP/TAZ cooperate with AP-1 to drive the mesenchymal cell state in neuroblastoma [CnR]

2025-10-02 | GSE275987 | GEO

YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-02-18 | GSE166943 | GEO

Widespread association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth [ChIP-Seq]

Project description:The goal of this study was to identify YAP/TAZ direct transcriptional targets and transcriptional partners, through ChIP-sequencing and gene expression profiling. ChIP-seq analysis of YAP, TAZ, TEAD4 and JUN in MDA-MB-231 cells. Two independent replicates were analysed for each TF, as well as for negative controls.

2015-08-03 | E-GEOD-66081 | biostudies-arrayexpress

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