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YAP and AP-1 cooperate to initiate rapid pancreatic cancer development from the ductal cell population in mice

ABSTRACT: YAP and AP-1 cooperate to initiate rapid pancreatic cancer development from the ductal cell population in mice

PROVIDER: PRJNA529863 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8812351_1.fastq.gz	Fastqsanger.gz
	SRR8812351_2.fastq.gz	Fastqsanger.gz
	SRR8812352_1.fastq.gz	Fastqsanger.gz
	SRR8812352_2.fastq.gz	Fastqsanger.gz
	SRR8812353_1.fastq.gz	Fastqsanger.gz

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YAP and AP-1 cooperate to initiate rapid pancreatic cancer development from the ductal cell population in mice

Project description:Purpose: We aimed to elucidate the unique consequences of YAP/TAZ activation in pancreatic ductal cells. Methods: We isolated RNA from Lats1 and Lats2 double knockout ductal cells from Lats1fl/fl; Lats2fl/fl; Sox9-CreER mice. Results: Oncogenic activation of YAP in ductal cells lead to the rapid development of carcinoma in situ with microinvasion.

2020-09-17 | GSE129045 | GEO

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

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 | GSE275987 | GEO

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

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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]

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

| PRJNA1154235 | ENA

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

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

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

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

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A non-canonical repressor function of JUN restrains YAP activity and suppresses YAP-dependent liver cancer growth [JUN_WT_M14_in_JUN_KO]

Project description:The transcriptional coactivators YAP/TAZ are the critical downstream regulators of the Hippo pathway that regulate gene expression in response to changes in pathway activity, mainly by binding to TEAD transcription factors. Uncontrolled transcriptional output of YAP/TAZ can lead to rapid induction of aggressive tumor growth. AP-1 is a dimeric basic leucine zipper (bZIP) transcription factor complex with JUN and FOS proteins being the most abundant members of this family. Unlike FOS, JUN can also form homodimers, but in the cell, JUN presumably preferentially forms heterodimers with members of the FOS family, which act as potent transcriptional activators. Previous studies identified substantial co-occupancy of YAP/TAZ and AP-1 at genomic sites, and they demonstrated that JUN/FOS heterodimers cooperate with the YAP/TAZ and TEAD transcription factors to drive YAP/TAZ target gene expression. Here, we now elucidate a negative feedback mechanism in which high YAP activity is restrained by the recruitment of homodimeric JUN::JUN/NCOR1 repressor complexes and show that this noncanonical JUN function is part of a tumor suppressor mechanism in the liver.

2024-06-30 | GSE235967 | GEO

A non-canonical repressor function of JUN restrains YAP activity and suppresses YAP-dependent liver cancer growth [iYAP5SA_10A_JUN_oe_antibodies_for_JUN_YAP_TEAD]

2024-06-30 | GSE235965 | GEO

A non-canonical repressor function of JUN restrains YAP activity and suppresses YAP-dependent liver cancer growth [CutRun_in_constitutive_5SA_MCF10A]

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