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Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway [DMSO vs DORMANT]

ABSTRACT: Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway [DMSO vs DORMANT]

PROVIDER: PRJNA544106 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9105260_1.fastq.gz	Fastqsanger.gz
	SRR9105260_2.fastq.gz	Fastqsanger.gz
	SRR9105270_1.fastq.gz	Fastqsanger.gz
	SRR9105270_2.fastq.gz	Fastqsanger.gz
	SRR9105261_1.fastq.gz	Fastqsanger.gz

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Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway [DMSO vs DORMANT]

Project description:Eradicating tumor dormancy that develops following oncogene-targeted therapy, including after epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) treatment of EGFR-mutant non-small cell lung cancer (NSCLC), is an attractive therapeutic strategy but the mechanisms governing the establishment of tumor dormancy are poorly understood. We observe that blockade of ERK1/2 reactivation following EGFR TKI treatment by combined EGFR/MEK inhibition uncovers cells that survive by entering a senescence-like dormant state, characterized by extensive epigenetic remodeling and high YAP/TEAD activity. YAP/TEAD trigger an epithelial-to-mesenchymal transition (EMT) program and engage the EMT transcription factor SLUG to directly repress pro-apoptotic BMF, limiting drug-induced apoptosis. Pharmacological co-inhibition of YAP or TEAD, or genetic deletion of YAP1, all deplete dormant cells by enhancing EGFR/MEK induced apoptosis. Thus, YAP activation can promote the survival of EGFR-mutant NSCLC cells in the chronic absence of EGFR signaling. Eradicating this population enhances the efficacy of targeted therapies which could ultimately lead to prolonged treatment responses in cancer patients.

2020-01-13 | GSE131594 | GEO

Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway [scRNASeq]

2020-01-13 | GSE138693 | GEO

Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway [ChIP + ATAC]

2020-01-13 | GSE131687 | GEO

Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway [YAP1 KO vs CTRL]

2020-01-13 | GSE131601 | GEO

Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway

Project description:Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway

| PRJNA544121 | ENA

Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway [scRNASeq]

Project description:Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway [scRNASeq]

| PRJNA576817 | ENA

Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway [ChIP + ATAC]

Project description:Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway [ChIP + ATAC]

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Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway [YAP1 KO vs CTRL]

Project description:Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway [YAP1 KO vs CTRL]

| PRJNA544119 | ENA

affy_sunflower_2010_13-ROS and hormones in sunflower seed dormancy.

Project description:affy_sunflower_2010_13 - affy_sunflower_2010_13 - It concerns the interaction between ROS and hormones in dormancy release in sunflower seeds. ABA is responsible for dormancy maintenance, while GA and ethylene promote seed germination. Based on our results, ROS could represent good candidate to shift from a hormone signalling to another determining the dormancy state in sunflower seeds.-We aim to understand the mechanisms controlling sunflower seed dormancy at the transcriptomic level, by the application of treatments which maintain dormancy as ABA, or alleviate dormancy as ROS and ethylene. Transcripts comparison will be performed between dormant and non-dormant sunflower embryo imbibed 24h on water, on ABA, on methylviologen, a pro-oxidant compound or on ethylene. 12 arrays - SUNFLOWER; treated vs untreated comparison

2013-08-01 | E-GEOD-44165 | biostudies-arrayexpress

Discrimination of dormant and active hematopoietic stem cells by G0 markers reveals dormancy regulation by cytoplasmic calcium

Project description:Quiescent hematopoietic stem cells (HSCs) are typically dormant, and only a few quiescent HSCs are active. The relationship between “dormant” and “active” HSCs remains unresolved. Here we generated a G0 marker (G0M) mouse line that visualizes quiescent cells. G0M identifies a small population of active HSCs (G0Mlow), which are distinct from dormant HSCs (G0Mhigh), within the conventional quiescent HSC fraction. Single-cell RNA-Seq analyses showed that the gene expression profiles of these populations were nearly identical, yet differed in their Cdk4/6 activity. Furthermore high-throughput small molecule screening revealed that high concentrations of cytoplasmic calcium ([Ca2+]c) were linked to dormancy of HSCs. These findings indicate that G0M separates dormant and active adult HSCs, which are regulated by Cdk4/6 and [Ca2+]c. This G0M mouse line represents a useful resource for investigating physiologically important stem cell subpopulations.

2019-12-20 | GSE139013 | GEO

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