YAP/TAZ-dependent expression of lncRNAs
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA856876 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20046731.fastq.gz | Fastqsanger.gz | |||
| SRR20046732.fastq.gz | Fastqsanger.gz | |||
| SRR20046733.fastq.gz | Fastqsanger.gz | |||
| SRR20046734.fastq.gz | Fastqsanger.gz | |||
| SRR20046735.fastq.gz | Fastqsanger.gz |
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Project description:Body fluids from cancer patients are informative regarding disease conditions in tumor tissues. Thus, biomarkers detected by liquid biopsy can guide clinicians in designing personalized therapies and may serve as a proxy for treatment success. However, biomarkers that predict the existence of druggable target structures cannot be reliably defined in blood samples due to genetic tumor heterogeneity and presence of molecules from non-tumorous cells. To test the applicability of RNA signatures as liquid biopsy biomarkers, expression data from hepatocellular carcinoma (HCC) cells after inhibition of Hippo pathway effectors is investigated. We show that the oncogene yes-associated protein (YAP) transcriptionally controls a panel of long non-coding RNAs (lncRNAs), which support HCC progression via tumor cell-intrinsic mechanisms. These lncRNAs are detectable and overexpressed in YAPS127A transgenic mouse livers as well as in a subgroup of human HCC tissue and serum samples. Using a machine learning algorithm, a 4 gene lncRNA signature is defined that correlates with the nuclear abundance of YAP in HCC tissues (CYTOR, SNHG1, SNHG17, MIR4435-2HG). Importantly, YAP accumulation in human HCCs is significantly associated with lncRNA signature serum abundance in two independent patient cohorts. Evaluation of expression data and confirmatory experiments illustrate that the lncRNA signature is a robust predictor for YAP activity in other tumor types such as lung adenocarcinoma. Liquid biopsy-based detection of lncRNAs in cancer patients is informative for the activity of transcriptional regulators and can serve as diagnostic tool that guides clinicians in the design of targeted therapies.
2023-03-15 | GSE207723 | GEO
Project description:Body fluids from cancer patients are informative regarding disease conditions in tumor tissues. Thus, biomarkers detected by liquid biopsy can guide clinicians in designing personalized therapies and may serve as a proxy for treatment success. However, biomarkers that predict the existence of druggable target structures cannot be reliably defined in blood samples due to genetic tumor heterogeneity and presence of molecules from non-tumorous cells. To test the applicability of RNA signatures as liquid biopsy biomarkers, expression data from hepatocellular carcinoma (HCC) cells after inhibition of Hippo pathway effectors is investigated. We show that the oncogene yes-associated protein (YAP) transcriptionally controls a panel of long non-coding RNAs (lncRNAs), which support HCC progression via tumor cell-intrinsic mechanisms. These lncRNAs are detectable and overexpressed in YAPS127A transgenic mouse livers as well as in a subgroup of human HCC tissue and serum samples. Using a machine learning algorithm, a 4 gene lncRNA signature is defined that correlates with the nuclear abundance of YAP in HCC tissues (CYTOR, SNHG1, SNHG17, MIR4435-2HG). Importantly, YAP accumulation in human HCCs is significantly associated with lncRNA signature serum abundance in two independent patient cohorts. Evaluation of expression data and confirmatory experiments illustrate that the lncRNA signature is a robust predictor for YAP activity in other tumor types such as lung adenocarcinoma. Liquid biopsy-based detection of lncRNAs in cancer patients is informative for the activity of transcriptional regulators and can serve as diagnostic tool that guides clinicians in the design of targeted therapies.
2023-03-15 | GSE207722 | GEO
Project description:The optic vesicle comprises a pool of bi-potential progenitor cells from which the retinal pigment epithelium (RPE) and neural retina fates segregate during ocular morphogenesis. Several transcription factors and signaling pathways have been shown to be important for RPE maintenance and differentiation, but an understanding of the initial fate specification and determination of this ocular cell type is lacking. We show that Yap/Taz-Tead activity is necessary and sufficient for optic vesicle progenitors to adopt RPE identity in zebrafish. A Teadresponsive transgene is expressed within the domain of the optic cup from which RPE arises, and Yap immunoreactivity localizes to the nuclei of prospective RPE cells. yap (yap1) mutants lack a subset of RPE cells and/or exhibit coloboma. Loss of RPE in yap mutants is exacerbated in combination with taz (wwtr1) mutant alleles such that, when Yap and Taz are both absent, optic vesicle progenitor cells completely lose their ability to form RPE. The mechanism of Yap dependent RPE cell type determination is reliant on both nuclear localization of Yap and interaction with a Tead co-factor. In contrast to loss of Yap and Taz, overexpression of either protein within optic vesicle progenitors leads to ectopic pigmentation in a dosagedependent manner. Overall, this study identifies Yap and Taz as key early regulators of RPE genesis and provides a mechanistic framework for understanding the congenital ocular defects of Sveinsson’s chorioretinal atrophy and congenital retinal coloboma. 60 pooled eyes from 36 hpf wild type or vsx2:Gal4/dsRed:14xUAS:YapS87A embryos were pooled for one sample. Three wild type and three vsx2:Gal4/dsRed:14xUAS:YapS87A pools were analyzed for RNA.
2015-08-06 | E-GEOD-71681 | biostudies-arrayexpress
Project description:The Hippo pathway effectors yes-associated protein (YAP) and WW domain containing transcription regulator 1 (TAZ/WWTR1) support tumor initiation and progression in various cancer types. However, to which extent YAP and TAZ cooperatively contribute to cholangiocarcinoma (CCA) development and progression is poorly understood. Our immunohistochemical studies showed that YAP and TAZ were expressed in different CCA subtypes. However, nuclear co-expression was not frequently detected. RNAinterference (RNAi) experiments illustrated that YAP and TAZ supported CCA cell viability. Comprehensive expression profiling of HUCCT-1 cells after combined silencing of YAP/TAZ revealed a potential impact on chromosomal instability.
2021-10-01 | GSE172135 | GEO
Project description:YAP/TAZ-dependent transcriptome in cholangiocarcinoma cells
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Project description:The Hippo pathway downstream effectors, Yap and Taz, play key roles in cell proliferation and tissue growth, regulating gene expression especially via interaction with Tead transcription factors. To investigate their role in skeletal muscle stem cells, we analysed gene expression changes driven by Taz and compared these to Yap mediated changes to the transcriptome by measurement of gene expression on Affymetrix microarrays. To interrogate overlapping and unique transcriptional changes driven by these Hippo effectors, satellite cell-derived myoblasts were transduced with constitutively active TAZ S89A or YAP S127A retrovirus for 24h or 48h, with empty retrovirus as control. Triplicate microarray analyses of empty vector controls, hYAP1 S127A and TAZ S89A transgenic primary myoblasts were conducted.
2017-06-20 | E-MTAB-5395 | biostudies-arrayexpress
Project description:The Hippo pathway plays a crucial in organ size control during development and tissue homeostasis in adult life. To examine a role for Hippo signaling in the intestinal epithelium, we analyzed gene expression patterns in the mouse intestinal epithelilum transfected with siRNAs or expression plasmids for shRNAs targeting the Hippo pathway effectors, YAP and TAZ. We performed two independent series of experiments (siGFP (n=3) vs siYAP/siTAZ (n=3), and shLacZ (n=1) vs shYAP/shTAZ (n=1)). Control siRNA (siGFP), YAP/TAZ siRNAs, or expression plasmids for control shRNA (shLacZ) or YAP/TAZ shRNAs were introduced into the mouse intestinal epithelium by the newly-developed in vivo transfection method. Four days after transfection, intestinal epithelial cells were isolated from the tissues and total RNA was extracted.
2014-07-18 | E-GEOD-45155 | biostudies-arrayexpress
Project description:Oral squamous cell carcinoma (OSCC) is a prevalent form of cancer that develops from the epithelium of the oral cavity. OSCC is on the rise worldwide, and death rates associated with the disease are particularly high. Despite progress in understanding of the mutational and expression landscape associated with OSCC, advances in deciphering these alterations for the development of therapeutic strategies have been limited. Further insight into the molecular cues that contribute to OSCC is therefore required. Here we show that the transcriptional regulators YAP (YAP1) and TAZ (WWTR1), which are key effectors of the Hippo pathway, drive pro-tumorigenic signals in OSCC. Regions of pre-malignant oral tissues exhibit aberrant nuclear YAP accumulation, suggesting that dysregulated YAP activity contributes to the onset of OSCC. Supporting this premise, we determined that nuclear YAP and TAZ activity drives OSCC cell proliferation, survival, and migration in vitro, and is required for OSCC tumor growth and metastasis in vivo. Global gene expression profiles associated with YAP and TAZ knockdown revealed changes in the control of gene expression implicated in pro-tumorigenic signaling, including those required for cell cycle progression and survival. Notably, the transcriptional signature regulated by YAP and TAZ significantly correlates with gene expression changes occurring in human OSCCs identified by The Cancer Genome Atlas (TCGA), emphasizing a central role for YAP and TAZ in OSCC biology. Expression profiling was conducted following the repression of the transcriptional regulators TAZ and YAP (YAP/TAZ) in human SCC2 oral cancer cells. Human SCC2 oral cancer cells were transfected with control siRNA, or siRNAs targeting TAZ, YAP, or YAP/TAZ for 48 hours. Total RNA from three independent experiments carried out on separate days was isolated and purified and the samples were then profiled on Affymetrix Human Gene 2.0 Chips at the Boston University Microarray Core. The expression profiles were processed and normalized using the Robust Multi-array Average (RMA) procedure (23) based on a custom Brainarray CDF (24). For each of the siRNA experiments, signatures of genes differentially expressed between treatment and corresponding siRNA control with an FDR q-value ?0.05 and a fold change ?2 were identified as either activated (up-regulated in control) or repressed (up-regulated in treatment). The overlap between the differentially expressed gene signatures was evaluated by Fisher test. Hierarchical gene and sample clustering was performed on the top 3000 genes with highest median absolute deviation (MAD; a robust version of the variance) across 12 samples, using “ward” as the agglomeration rule, and 1 minus Pearson correlation and Euclidean as the distance measures for genes and samples, respectively.
2015-05-26 | E-GEOD-66949 | biostudies-arrayexpress