Expression data from Mammospheres
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE35899 | GEO | 2014/02/18
SECONDARY ACCESSION(S): PRJNA151995
REPOSITORIES: GEO
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Project description:The combined activation of Wnt/ß-catenin and MET/HGF is required for mammary cancer stem cell (MaCSC) maintenance. We generated mammospheres derived from tumors of mice harboring Wnt/Met signaling mutations on which we performed microarray analysis to evaluate gene expression signatures controlled by Wnt and MET pathways. We used the gene expression profiles to dissect the role and the functions of these pathways in MaCSCs. We treated mammospheres with Wnt and MET pathway inhibitors (ICG-001 and PHA665752 respectively) alone or in combination. Samples treated with DMSO were used as vehicle control.
2014-02-18 | E-GEOD-35899 | biostudies-arrayexpress
Project description:Co-occurrence of aberrant hepatocyte growth factor (HGF)/MET proto-oncogene receptor tyrosine kinase (MET) and Wnt/β-catenin signaling pathways has been observed in advanced and metastatic prostate cancers. This co-occurrence positively correlates with prostate cancer progression and castration-resistant prostate cancer (CRPC) development. However, the biological consequences of these abnormalities in these disease processes remain largely unknown. Here, we investigated the aberrant activation of HGF/MET and Wnt/β-catenin cascades in prostate tumorigenesis by using a newly generated mouse model in which both murine Met transgene and stabilized β-catenin are conditionally co-expressed in prostatic epithelial cells. These compound mice displayed accelerated prostate tumor formation and invasion compared with their littermates that expressed only stabilized β-catenin.RNA-Seq and qRT-PCR analyses revealed increased expression of genes associated with tumor cell proliferation, progression,and metastasis. Moreover, Wnt signaling pathways were robustly enriched in prostate tumor samples from the compound mice.ChIP-qPCR experiments revealed increased β-catenin recruitment within the regulatory regions of the Myc gene in tumor cellsof the compound mice. Interestingly, the occupancy of MET on the Myc promoter also appeared in the compound mouse tumor samples,implicating a novel role of MET in β-catenin–mediated transcription. Results from implanting prostate graft tissues derived from the compound mice and controls into HGF-transgenic mice further uncovered that HGF induces prostatic oncogenic transformation and cell growth. These results indicate a role of HGF/MET in β-catenin–mediated prostate cancer cell growth and progressionand implicate a molecular mechanism whereby nuclear MET promotes aberrant Wnt/β-catenin signaling–mediated prostate tumorigenesis.
2019-12-17 | GSE142158 | GEO
Project description:CSCs may be regulated by extrinsic signals provided by specialized microenvironments, or niches, which sustain CSC expansion. We investigated the role of cancer associated fibroblasts (CAFs) in the regulation of CSCs using a genetically engineered mouse model of basal-like breast cancer driven by combined activation of Wnt/β-catenin and HGF/Met signaling (Wnt-Met mice). We found that CAFs secrete soluble factors that promote the expansion of the population of self-renewing cells that generate mammospheres and enhance the capacity of CSCs to form invasive 3D structures. Using transcriptional profiling, we identified a network of paracrine interactions between CAFs and CSCs that regulate reciprocal functions.
2018-04-23 | GSE68241 | GEO
Project description:Genetic and epigenetic defects in Wnt/ß-catenin signaling play important roles in colorectal cancer progression. Here we identify DACT3, a member of the DACT (Dpr/Frodo) gene family, as a negative regulator of Wnt/ß-catenin signaling that is transcriptionally repressed in colorectal cancer. Unlike other Wnt signaling inhibitors that are silenced by DNA methylation, DACT3 repression is associated with bivalent histone modifications. Remarkably, DACT3 expression can be robustly de-repressed by a pharmacological combination that simultaneously targets both histone methylation and deacetylation, leading to strong inhibition of Dishevelled (Dvl)-mediated Wnt/ß-catenin signaling and massive apoptosis of colorectal cancer cells. Our study identifies DACT3 as an important regulator of Wnt/ß-catenin signaling in colorectal cancer and suggests a potential strategy for therapeutic control of Wnt/ß-catenin signaling in colorectal cancer. Keywords: Colon cancer cell line
2008-03-29 | GSE10952 | GEO
Project description:Tumorpsheres and mammospheres were used to propagate mouse breast tumor-initiating cells and their normal stem/progenitor counterparts, respectively. Mammospheres induced to differentiate were used to model the more differentiated cells of the mouse mammary gland. We used microarrays to find differentrially expressed genes between tumorspheres, mammospheres, and mammospheres induced to differentiate
2012-01-30 | GSE32463 | GEO
Project description:24 colon normal and tumor pairs using Illumina BeadChip Human Ref8-v2. Genetic and epigenetic defects in Wnt/ß-catenin signaling play important roles in colorectal cancer progression. Here we identify DACT3, a member of the DACT (Dpr/Frodo) gene family, as a negative regulator of Wnt/ß-catenin signaling that is transcriptionally repressed in colorectal cancer. Unlike other Wnt signaling inhibitors that are silenced by DNA methylation, DACT3 repression is associated with bivalent histone modifications. Remarkably, DACT3 expression can be robustly de-repressed by a pharmacological combination that simultaneously targets both histone methylation and deacetylation, leading to strong inhibition of Dishevelled (Dvl)-mediated Wnt/ß-catenin signaling and massive apoptosis of colorectal cancer cells. Our study identifies DACT3 as an important regulator of Wnt/ß-catenin signaling in colorectal cancer and suggests a potential strategy for therapeutic control of Wnt/ß-catenin signaling in colorectal cancer. The clinical information for the colon tumor is not available. Keywords: human colon tumor
2008-03-29 | GSE10950 | GEO
Project description:Transcription profiling by array of mammospheres derived from tumors of mice harboring Wnt/Met signaling mutations treated Wnt and MET pathway inhibitors
2014-11-07 | E-GEOD-35899 | ExpressionAtlas
Project description:Context dependent molecular cues shape the formation of the cerebral vascular network and the function of the blood-brain barrier (BBB). The Wnt/ß-catenin pathway is orchestrating CNS vascular development, but downstream mediators have not been characterized. Here we generated an endothelial cell-specific R26-Axin1 overexpression (AOE) mouse model to inhibit Wnt/ß-catenin signaling. In AOE mice we discovered that blockade of Wnt/ß-catenin pathway leads to premature regression and remodeling without compromising BBB integrity. Importantly, by comparing transcriptomes of endothelial cells from wildtype and AOE mice, we identified ADAMTSL2 as a novel Wnt/ß-catenin-induced, secreted factor, important for stabilizing the BBB during development. Zebrafish loss-of-function and gain-of-function models, further demonstrated that ADAMTSL2 is crucial for normal vascular development and could rescue vascular phenotypes in AOE zebrafish brains. In conclusion, the studies presented here reveal a hitherto unrecognized role of ADAMTSL2 as an endothelial cell-specific mediator of Wnt/ß-catenin signaling during CNS vascular development and BBB-formation.
2019-02-22 | GSE66848 | GEO
Project description:Tumorpsheres and mammospheres were used to propagate mouse breast tumor-initiating cells and their normal stem/progenitor counterparts, respectively. Mammospheres induced to differentiate were used to model the more differentiated cells of the mouse mammary gland. We used microarrays to find differentrially expressed genes between tumorspheres, mammospheres, and mammospheres induced to differentiate Primary cells were isolate from either mouse mammary glands (FVB/N) or mouse mammary tumors and placed in stem cell media (MMTV-Neu [N2O2]. Spheres were passaged every 7 days for 3-5 passages and harvested for RNA isolation
2012-01-30 | E-GEOD-32463 | biostudies-arrayexpress
Project description:Genetic and epigenetic defects in Wnt/?-catenin signaling play important roles in colorectal cancer progression. Here we identify DACT3, a member of the DACT (Dpr/Frodo) gene family, as a negative regulator of Wnt/ß-catenin signaling that is transcriptionally repressed in colorectal cancer. Unlike other Wnt signaling inhibitors that are silenced by DNA methylation, DACT3 repression is associated with bivalent histone modifications. Remarkably, DACT3 expression can be robustly de-repressed by a pharmacological combination that simultaneously targets both histone methylation and deacetylation, leading to strong inhibition of Dishevelled (Dvl)-mediated Wnt/?-catenin signaling and massive apoptosis of colorectal cancer cells. Our study identifies DACT3 as an important regulator of Wnt/ß-catenin signaling in colorectal cancer and suggests a potential strategy for therapeutic control of Wnt/ß-catenin signaling in colorectal cancer. This SuperSeries is composed of the SubSeries listed below.
2008-03-29 | GSE10972 | GEO