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RNA-seq on MCF10A-YAP cells (overexpressed constrictively activated YAP in MCF10A cells) transduced with sgRNAs vectors targeting TRAM2 gene

ABSTRACT: We performed a CRISPR-based functional genetic screen targeting TEAD4 binding motif located within the YAP-bound enhancers. The screen identified a novel enhancer regulating TRAM2. We observed TRAM2 overexpression can induce EMT as YAP does. Then, we performed the RNA-seq to measure the transcription changes upon TRAM2-KOs in MCF10A-YAP cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE147556 | GEO | 2020/06/01

REPOSITORIES: GEO

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RNA-seq on MCF10A-YAP5SA cells (overexpressed constrictively activated YAP in MCF10A cells) transduced with sgRNAs vectors targeting the TEAD4 binding motif within the identified enhancers

Project description:We performed a CRISPR-based functional genetic screen targeting TEAD4 binding motif located within the YAP-bound enhancers. The screen identified seven functional enhancers whose targeting resulted in a marked negative effect on the proliferation of MCF10A-YAP-5SA cells (overexpressed constrictively activated YAP) but no significant effect on MCF10A (parental control) cells. We then carried out RNA-seq analysis on MCF10A-YAP-5SA cells transduced with sgRNA vectors targeting these seven enhancers (enhancers A, B, C, D, E, F, G) as well as the non-targeting sgRNA as control (NT).

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RNA-seq on MCF10A cells overexpressed with empty control vectors, TRAM2 and activated-YAP

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RNA-seq on MCF10A-YAP cells (overexpressed constrictively activated YAP in MCF10A cells) transduced with sgRNAs vectors targeting TRAM2 gene

Project description:RNA-seq on MCF10A-YAP cells (overexpressed constrictively activated YAP in MCF10A cells) transduced with sgRNAs vectors targeting TRAM2 gene

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RNA-seq on MCF10A-YAP5SA cells (overexpressed constrictively activated YAP in MCF10A cells) transduced with sgRNAs vectors targeting the TEAD4 binding motif within the identified enhancers

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Transcription profiling by array of human MCF10A cells expressing YAP to identify the targets of the YAP oncogene

Project description:YAP is an oncogene and an inducer of Epithelial-to-Mesenchymal Transition (EMT). We used microarrays to detail the global program of gene expression to identify YAP target genes. PUBLICATION ABSTRACT:; The Hippo pathway defines a novel signaling cascade regulating cell proliferation and survival in Drosophila, which involves the negative regulation of the transcriptional coactivator Yorkie by the kinases Hippo and Warts. We have recently shown that the human ortholog of Yorkie, YAP, maps to a minimal amplification locus in mouse and human cancers, and that it mediates dramatic transforming activity in MCF10A primary mammary epithelial cells. Here we show that LATS proteins (mammalian orthologs of Warts) interact directly with YAP in mammalian cells and that ectopic expression of LATS1, but not LATS2, effectively suppresses the YAP phenotypes. Furthermore, shRNA-mediated knockdown of LATS1 phenocopies YAP overexpression. Since this effect can be suppressed by simultaneous YAP knockdown, it suggests that YAP is the primary target of LATS1 in mammalian cells. Expression profiling of genes induced by ectopic expression of YAP or by knockdown of LATS1 reveals a subset of potential Hippo pathway targets implicated in epithelial-to-mesenchymal transition (EMT), suggesting that this is a key feature of YAP signaling in mammalian cells. Experiment Overall Design: MCF10A cells were infected with retrovirus constructs (vector or YAP) and puromycin was used to select for transduced cells. Cells were split and grown to ~60-75%% confluency at which point they were harvested for RNA. Vector vs. YAP comparison was done in duplicate.

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Transcription profiling of human YAP wild-type or mutants overexpressing MCF10A cells

Project description:This study compares gene expression change upon expression of Yes-associated protein (YAP) wild-type or mutants in order to establish the importance of TEAD binding and WW domains in the gene-induction function of YAP. The results indicate that gene-induction is seriously comprised in YAP-S94A (TEAD binding domain mutant) expressing cells. And mutantion of WW domains (YAP-W1W2) also affect a fraction of YAP induced genes. Therefore both TEAD binding domain and WW domains are required for the full function of YAP in gene-induction. Experiment Overall Design: Four samples are included: 1. pQCXIH vector control; 2 YAP-WT expression; 3. YAP-S94A expression; 4. YAP-W1W2 expression. Gene expression profiles of YAP wild-type or mutants expressing cells were compared to that of vector control. Experiments were done in MCF10A mammary epithelial cells.

2010-01-19 | E-GEOD-13218 | biostudies-arrayexpress

ChIP-seq analysis of MCF10A cells exressing active mutant YAP-5SA

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A comprehensive enhancer screen identifies TRAM2 as a key mediator of YAP oncogenesis

Project description:Frequent activation of the co-transcriptional factor YAP is observed in a large number of solid tumors. Activated-YAP associates with enhancer loci via TEAD4-DNA-binding protein, and stimulates cancer aggressiveness. Although thousands of YAP/TEAD4 binding-sites were annotated, their functional importance is unknow. Here, we implemented a genetic approach to uncover functions of YAP/TEAD4-associated enhancers, demonstrated its robustness, and used it to reveal a network of enhancers required for YAP-mediated proliferation. We focused on Enhancer TRAM2, as its target gene TRAM2 showed the strongest expression-correlation with YAP in nearly all tumor types. Interestingly, TRAM2 phenocopied YAP-induced cell proliferation, migration and invasion phenotypes, and correlated with poor patient survival. Mechanistically, we identified FSTL-1 as a major direct client of TRAM2 that is involved in these phenotypes. Thus, TRAM2 is a key novel mediator of YAP-induced oncogenic proliferation and cellular invasiveness.

2021-01-14 | PXD018559 | Pride

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