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

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

PROVIDER: PRJNA544119 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9105480.fastq.gz	Fastqsanger.gz
	SRR9105490.fastq.gz	Fastqsanger.gz
	SRR9105500.fastq.gz	Fastqsanger.gz
	SRR9105481.fastq.gz	Fastqsanger.gz
	SRR9105491.fastq.gz	Fastqsanger.gz

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

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 | GSE131601 | GEO

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

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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 [DMSO vs DORMANT]

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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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Regulation of gene expression by YAP1

Project description:In order to define YAP1-specific gene expression patterns in gastric cancer, the constitutively active mutant YAP1 (YAP1-S127A) was over-expressed in MKN45 gastric cancer cells. Defined gene expression signature was later used to stratify gastric cancer patients according to the presence of the YAP1-activated signature. Three groups of samples are included: 1. Mock control; 2. Vector control; 3. YAP-S127A expression. Gene expression profiles of YAP-S127A mutant-expressing cells were compared to that of mock and vector control. Experiments were done in MKN45 gastric cancer cells.

2013-10-01 | E-GEOD-41387 | biostudies-arrayexpress

Effect of YAP overexpression on HuCCT1 cholangiocarcinoma cell line transcriptome (YAP overexpression)

Project description:The YAP pathway in regulating organ size by integrating external signals to control the expression of genes involved in cell proliferation. YAP is known to be involved in tumorigenesis in several tissues, yet its role in cholangiocarcinoma is not established We used microarrays to assess the role of YAP pathway in cholangiocarcinoma either by overexpressing a constitutively active YAP1 mutant, or by downregulating YAP1 expression using shRNA HuCCT1 cells where transfected with either an empty vector or a vector overexpressing the constitutively active YAP1 S127A; cells were harvested, RNA was collected and analyzed using microarray

2015-10-27 | E-GEOD-61764 | biostudies-arrayexpress

Effect of YAP overexpression on HuCCT1 cholangiocarcinoma cell line transcriptome (shRNA targeting YAP)

Project description:The YAP pathway in regulating organ size by integrating external signals to control the expression of genes involved in cell proliferation. YAP is known to be involved in tumorigenesis in several tissues, yet its role in cholangiocarcinoma is not established We used microarrays to assess the role of YAP pathway in cholangiocarcinoma either by overexpressing a constitutively active YAP1 mutant, or by downregulating YAP1 expression using shRNA HuCCT1 cells where transfected with either a control scrambled shRNA or a shRNA targeting YAP1; cells were harvested, RNA was collected and analyzed using microarray

2015-10-27 | E-GEOD-61765 | biostudies-arrayexpress

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