Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

46 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression Data from Normal or ErbB2 Tumor Fibroblasts With or Without Ets2

ABSTRACT: The mechanisms involved in epithelium-stroma interactions remain poorly understood, despite the importance of the microenvironment during tumorigenesis. Here, we studied the role of Ets2 transcrpiton factor in tumor associated fibroblasts in the MMTV-ErbB2 mammary tumor model. Inactivation of Ets2 specifically in fibroblasts using Fsp-cre significantly reduced tumor growth, in contrast to Ets2 inactivation in epithelium in which no differences in tumor growth were observed. Microarray analysis on isolated fibroblasts demonstrated the important role of Ets2 in remodeling of the extracellular matrix and angiogenesis in these cells. Tumors lacking Ets2 in fibroblats had diminished blood vessels. Our tumor specific gene signature was also represented in the stroma of human breast cancer patients. Collectively, our results suggest Ets2 uniquely contributes to angiogenesis from fribroblasts in the tumor microenvironment. Primary mammary fibroblasts were isolated from mice with no oncogene with or without Ets2 and with the ErbB2 oncogene with or without Ets2, RNA was extracted and samples were submitted for Affymetrix gene expression arrays

ORGANISM(S): Mus musculus

SUBMITTER: Julie Wallace

PROVIDER: E-GEOD-44166 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Expression Data from Normal or Tumor Fibroblasts With or Without Ets2

Project description:The mechanisms involved in epithelium-stroma interactions remain poorly understood, despite the importance of the microenvironment during tumorigenesis. Here, we studied the role of the Ets2 transcription factor in tumor-associated fibroblasts in the MMTV-PyMT mammary tumor model. Inactivation of Ets2 specifically in fibroblasts using Fsp-cre significantly reduced tumor growth, in contrast to Ets2 inactivation in epithelium, in which no differences in tumor growth were observed. Microarray analysis on isolated fibroblasts demonstrated the important role of Ets2 in remodeling of the extracellular matrix and angiogenesis in these cells. At the molecular level, Ets2 regulated Mmp9 expression through direct binding to the promoter region. Tumors lacking Ets2 in fibroblasts had diminished blood vessels. We also found a significant correlation between phosphorylation of ETS2 and MMP9 levels in stroma of human breast cancer samples. Collectively, our results suggest Ets2 uniquely contributes to angiogenesis from fibroblasts in the tumor microenvironment. Primary mammary fibroblasts were isolated from mice without the PyMT oncogene with or without Ets2, and from mice with the PyMT oncogene with or without Ets2. RNA was extracted and samples were submitted for Affymetrix gene expression arrays.

2014-03-19 | E-GEOD-16989 | biostudies-arrayexpress

Expression Data from Normal or ErbB2 Tumor Fibroblasts With or Without Ets2

Project description:The mechanisms involved in epithelium-stroma interactions remain poorly understood, despite the importance of the microenvironment during tumorigenesis. Here, we studied the role of Ets2 transcrpiton factor in tumor associated fibroblasts in the MMTV-ErbB2 mammary tumor model. Inactivation of Ets2 specifically in fibroblasts using Fsp-cre significantly reduced tumor growth, in contrast to Ets2 inactivation in epithelium in which no differences in tumor growth were observed. Microarray analysis on isolated fibroblasts demonstrated the important role of Ets2 in remodeling of the extracellular matrix and angiogenesis in these cells. Tumors lacking Ets2 in fibroblats had diminished blood vessels. Our tumor specific gene signature was also represented in the stroma of human breast cancer patients. Collectively, our results suggest Ets2 uniquely contributes to angiogenesis from fribroblasts in the tumor microenvironment.

2013-12-01 | GSE44166 | GEO

Expression Data from Normal or Tumor Fibroblasts With or Without Ets2

2014-03-19 | GSE16989 | GEO

Expression Data from Endothelial Cells as a Consequence of Ets2 Signaling in PyMT Tumor Associated Fibroblasts

Project description:Tumor associated fibroblasts are known to play an important role in angiogenesis, however the specific signaling pathways playing an important role in this cross talk remain ill defined. Here, we studied how Ets2 transcrpiton factor signaling in tumor associated fibroblasts effected gene expression in surrounding endothelial cells in the MMTV-PyMT mammary tumor model. Inactivation of Ets2 specifically in fibroblasts using Fsp-cre significantly reduced tumor associated angiogenesis, and was indicated to effect ECM remodeling, cell adhesion and cell chemotaxis processes in neighboring endothelial cells. We have identified Ets2 in fibroblasts as a key signaling molecule to induce tumor associated angiogenesis. Additionally, this function does not rely on the presence of tumor cells, indicating a memory in fibroblasts to induce angiogenesis. Primary mammary endothelial cells were isolated from mice with or without fibroblast Ets2 in the presence of the PyMT oncogene through sorting with a CD31 antibody. RNA was extracted and samples were submitted for Affymetrix gene expression arrays

2013-12-01 | E-GEOD-44118 | biostudies-arrayexpress

Transcription profiling of mouse Pten Null Fibroblasts

Project description:The tumor stroma is believed to contribute to some of the most malignant characteristics of epithelial tumors. However, signaling between stromal and tumor cells is complex and remains poorly understood. Here we show that genetic inactivation of Pten in stromal fibroblasts of mouse mammary glands accelerated the initiation, progression and malignant transformation of mammary epithelial tumors. Global gene expression profiling in mammary stromal cells identified a Pten-specific signature associated with massive extra-cellular matrix (ECM) remodeling, innate immune cell infiltraion and increased angiogenesis. Execution of this transcriptional program was mediated, in part, by the induction, phosphorylation and recruitment of Ets2 to target promoters. Remarkably, Ets2 inactivation in Pten stroma-deleted tumors was sufficient to decrease tumor growth and progression. These findings identify the Pten-Ets2 axis as a critical stroma-specific signaling pathway that suppresses mammary epithelial tumors. Experiment Overall Design: Wild type and Pten null primary mammary fibroblasts isolated from 8 week old female mice were cultured, RNA was extracted and Affymetrix gene expression arrays were performed.

2009-11-10 | E-GEOD-16073 | biostudies-arrayexpress

Expression Data from Pten Null Fibroblasts

2009-10-22 | GSE16073 | GEO

Expression Data from Endothelial Cells as a Consequence of Ets2 Signaling in PyMT Tumor Associated Fibroblasts

2013-12-01 | GSE44118 | GEO

Gene expression profile of the mammary stroma in Rarb -/- mice compared to their wild type littermates

Project description:Inactivation of RAR-b, which has been reported as a tumor suppressing gene by numerous studies, results in protective effect against the tumorigenesis induced by activated ErbB2. Moreover, tissue recombination indicates that the RAR-b deficient-microenvironment, rather than the RAR-b status of mammary epithelial cells, plays a key-determining role in the initiation and progression of the mammary carcinoma. Ablation of RAR-b extensively modulates the remodeling of stroma during tumor progression through suppressing the activation and transdifferetiation of myofibroblasts. RNA microarray has been employed to identify the gene expression signature in the mammary stroma of our RAR-b null animals. We want to find out the underlining mechanism of the protective effects resulted from Rarb abliton. A global gene expression profile of mouse mammary stroma was obtained on total RNA from the cleared mammary fat pads (stroma) of both RAR-b KO (n=3) and their wild type (n=3) littermates at the age of four weeks.

2010-12-18 | E-GEOD-19925 | biostudies-arrayexpress

Gene expression profile of the mammary stroma in Rarb -/- mice compared to their wild type littermates

2010-12-18 | GSE19925 | GEO

Gene expression of spheres made from mammary tumors of FRS2b hetero mice and knock-out mice

Project description:Precancerous tissue microenvironment is thought to be important for tumorigenesis when cancer stem-like cells (CSCs) begin to grow, though underlying mechanisms remain unclear. Here, we uncovered critical roles of luminal progenitor cells expressing FRS2β, an inhibitory adaptor for ErbB signaling, to create the cytokines-rich CSC niche in mammary tissues. Deficiency of FRS2β greatly decreased mammary tumorigenesis with decreased tumor stroma in mouse mammary tumor virus (MMTV)-ErbB2 mice. Moreover, FRS2β-deficient precancerous mammary tissues did not allow tumorigenesis derived from xenografted wild type FRS2β tumor cells. Insulin-like growth factor (IGF) 1 and CXC chemokine ligand (CXCL) 12, stemness- and stroma-inducing cytokines, respectively, were expressed at low levels in FRS2β-deficient precancerous mammary cells. Treatment with inhibitors against these cytokines in precancerous mice greatly decreased tumorigenic potential. In addition, human breast cancer tissues in which FRS2β is highly expressed in tumor cells harbor more stroma, and are associated with poor prognosis. Thus, cytokines-rich CSC niche and tumor microenvironment induced by FRS2β expressed in luminal progenitor cells and tumor cells play important roles for tumorigenesis.

2021-09-07 | GSE120034 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data