Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

16 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PTHR1 knock-down in osteosarcoma cells

ABSTRACT: Expression analysis of OS tumors with shRNA knockdown of PTHR1 mouse OS 80 (a Cre:lox OS cell line from Boston) was tagged with firefly luciferase expression construct. They were then infected with either control (renilla luciferase shRNA) or an shRNA that effective knocks-down PTHR1 (PTHR1.358; para-thyroid hormone receptor). The cells were injected with matrigel onto the back flank of Balb/c nu/nu mice and left to grow for 1 month with weekly monitoring of tumour size by in vivo luciferase assay. At 4 weeks the tumours were removed and trizol stored. Whole tumour was ground up and set form micro-array. 6 tumors with shRNA PTHR1 knockdown ; 6 tumors with shRNA control (renilla luciferase shRNA) knockdown

ORGANISM(S): Mus musculus

SUBMITTER: Alistair Chalk

PROVIDER: E-GEOD-46861 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Modeling tumor subtypes in vivo using lineage restricted transgenic shRNA

Project description:Expression analysis from two genetically engineered mouse models of osteosarcoma determine the expression profile of mouse osteosarcoma Human osteosarcoma (OS) is comprised of three different subtypes: fibroblastic, chondroblastic and osteoblastic. We previously generated a mouse model of fibroblastic OS by conditional deletion of p53 and Rb in osteoblasts. Here we report an accurate mouse model of the osteoblastic subtype using shRNA-based suppression of p53. Like human OS, tumors frequently present in the long bones and preferentially disseminate to the lungs; features less consistently modeled using Cre:lox approaches. Our approach allowed direct comparison of the in vivo consequences of targeting the same genetic drivers using different technology. This demonstrated that the effects of Cre:lox and shRNA mediated knock-down are qualitatively different, at least in the context of osteosarcoma. Through the use of complementary genetic modification strategies we have established a model of a distinct clinical subtype of OS that was not previously represented and more fully recapitulated the clinical spectrum of this human tumor. 4 primary tumors from Cre:lox OS model; 4 primary tumors from shRNA OS model.

2013-03-28 | E-GEOD-38742 | biostudies-arrayexpress

Wnt inhibitory factor 1 (WIF1) is a marker of osteoblastic differentiation stage and is not silenced by DNA methylation in osteosarcoma

Project description:Purpose: We have used microarrays to identify gene expression profiles that distinguish mouse OS cells from normal pre-osteoblast cells and mature osteoblast cells. Methods: Transcriptional profiles of three cell lines derived from tumors from Osx-Cre p53fl/fl Rbfl/fl (fibroblastic OS) mouse model, and from pre-osteoblast cells (Kusa4b10 mouse bone marrow stromal cell line) and osteoblast cells (derived by in vitro differentiation of the Kusab410 mouse bone marrow stromal cell line) were generated by microarray analysis, each in triplicate, using Affymetrix mouse Gene1.0ST arrays. Transcriptional profiles were analyzed in cell lines derived from tumors from a genetically engineered mouse model of human osteosarcoma (Osx-Cre p53fl/fl Rbfl/fl) and osteoblast cells derived from the Kusa4b10 mouse bone marrow stromal cell line, in the undifferentiated state (pre-osteoblasts) and differentiated state (osteoblasts).

2015-01-29 | E-GEOD-63939 | biostudies-arrayexpress

Wnt inhibitory factor 1 (WIF1) is not silenced by DNA methylation in osteosarcoma, and instead, represents a marker of osteoblastic differentiation stage (gene expression)

Project description:The aim was to identify pathways and genes that are transcriptionally deregulated in osteosarcoma due to changes in CpG island DNA methylation. In order to identify candidates, we compared low passage cell cultures derived from a mouse model of osteosarcoma to mature osteoblasts derived by in vitro differentiation of the mouse bone marrow stromal cell line, Kusa4b10. Under cell culture osteoblastic differentiating conditions, Kusa4b10 cells acquire a mature osteoblastic phenotype (21 days). A potential role for DNA methylation in directing gene expression changes was established by integrating gene expression data with genome wide DNA methylation maps generated by methyl-DNA binding domain capture and NimbleGen promoter arrays (MBDCap-Chip). 3 cell lines derived from primary tumors from p53 Rb Osterix-Cre:lox OS model, 3 Osteoblasts (differentiated Kusa4b10 cells (21 days under osteoblastic differentiation conditions)

2015-07-01 | E-GEOD-46929 | biostudies-arrayexpress

RNA editing by ADAR1 is essential for erythropoiesis [array]

Project description:Erythroid progenitors purified from EpoRCreR26eYFPADAR1fl/- and EpoRCreR26eYFPADAR1fl/+ control mice were compared for global gene array profiles Each sample was purified from one mouse

2016-07-24 | E-GEOD-59664 | biostudies-arrayexpress

ADAR1-mediated A-to-I RNA editing is essential for erythropoiesis

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-07-24 | E-GEOD-71047 | biostudies-arrayexpress

Overexpression of cSki in hematopoietic stem and progenitor cells

Project description:Human cSki was overexpressed using MIGR1 retrovirus in sorted murine Lin-c-Kit+Sca-1+ cells. Cells were infected and cultured for 2 days after infection prior to isolation of GFP+ve cells and microarray. GFP+ve MIGR1 and cSKI cells were compared. Each sample represents an independent infection with either cSki or MIGR1 Comparison of GFP+ve LKS+ infected with MIGR1 and cSki

2014-01-21 | E-GEOD-39457 | biostudies-arrayexpress

RNA Sequencing Quantitative Analysis of cell lines derived from tumours from two mouse models of human osteosarcoma that recapitulate clinically distinct human osteosarcoma subtypes.

Project description:Purpose: Osteosarcoma (OS) is the most common primary bone malignancy. OS consists of several subtypes including fibroblastic, osteoblastic and chondroblastic OS. We have developed genetically engineered mouse models of human OS that recapitulate two distinct subtypes, fibroblastic (Osx-CreLox p53-/- Rb-/-) and osteoblastic (Osx-Cre shRNA p53-/-) OS. The goal of this study was to identify transcriptional differences that distinguish the two subtypes. Methods: mRNA profiles of cell lines derived from tumours from Osx-Cre p53fl/fl Rbfl/fl (fibroblastic OS) and Osx-Cre shRNA TRE-p53.1224 pRbfl/fl (osteoblastic OS) mouse models were generated by RNA sequencing, in triplicate, using Illumina HiSeq2000. The sequence reads that passed quality filters were analyzed at the transcript level with TopHat followed by Cufflinks. Results: Using an optimized data analysis workflow, we mapped about 30 million sequence reads per sample to the mouse genome (build mm9) and identified 12,436 transcripts in the tumours of Osx-Cre p53fl/fl Rbfl/fl and 12,074 Osx-Cre shRNA TRE-p53.1224 pRbfl/fl with the TopHat workflow. RNA-seq data confirmed stable expression of 25 known housekeeping genes. Conclusions: Our study represents a detailed analysis of OS subtype transcriptomes generated by RNA-seq technology. mRNA profiles of cell lines derived from tumours from two genetically engineered mouse models of human osteosarcoma (Osx-Cre p53fl/fl Rbfl/fl and Osx-Cre shRNA TRE-p53.1224 pRbfl/fl) were generated by deep sequencing, in triplicate, using Illumina HiSeq 2000.

2015-07-06 | E-GEOD-58916 | biostudies-arrayexpress

Oxidoreductase transcript data from human umbilical vein endothelial cells

Project description:Oxidoreductase enzymes are critical to redox regulation of intracellular proteins within human cells. We used microarrays to identify which oxidreducatse genes are expressed in unstimulated human umbilical vein endothelial cells. Human umbilical vein endothelial cells were grown under optimal conditions and then RNA extracted and hybridized on Affymetrix microarrays.

2010-06-16 | E-GEOD-22166 | biostudies-arrayexpress

The ets transcription factor ELF5 suppresses the estrogen sensitive phenotype and contributes to antiestrogen resistance in luminal breast cancer. [mouse]

Project description:The ets transcription factor ELF5 specifies the differentiation of mammary progenitor cells to establish the milk-secreting lineage. ER- and poor prognosis basal breast cancers arise from this progenitor cell and these cancers express high levels of Elf5. Knockdown of ELF5 expression in basal breast cancer cell lines, or forced expression in luminal breast cancer cell lines, resulted in reduced cell proliferation. Transcript profiling and chromatin immunoprecipitation revealed that the transcriptional activity of ELF5 specified the gene expression patterns that distinguish basal from luminal breast cancer, including suppression of FOXA1, GATA3 and ER, key estrogen-action genes. Tamoxifen treatment of luminal MCF7 cells upregulated Elf5 expression and cells that acquired resistance to Tamoxifen became dependent on ELF5 for proliferation. ELF5 is a regulator of breast cancer cell proliferation, transcriptionally specifies the basal molecular subtype and is utilised by ER+ breast cancer cells to escape proliferative arrest caused by Tamoxifen. Elf5 was induced via doxycycline treated PyMT mouse tumours, in triplicate

2014-01-13 | E-GEOD-30406 | biostudies-arrayexpress

A Myc transcriptional program that is independent of EMT drives a poor prognosis tumor-propagating phenotype in HER2+ breast cancer

Project description:The HER2 (ERBB2) and MYC genes are commonly amplified genes in breast cancer, yet little is known about their molecular and clinical interaction. Using a novel chimeric mammary transgenic approach and in vitro models, we demonstrate markedly increased self renewal and tumour propagating capability of cells transformed with Her2 and c-Myc. Co-expression of both oncogenes in cultured cells led to a pronounced activation of a c-Myc transcriptional signature and acquisition of a self renewing phenotype independent of an EMT programme or regulation of cancer stem cell markers. We show that HER2 and c-MYC are frequently co-amplified in a clinical breast cancer cohort and that co-amplification is strongly associated with aggressive clinical behaviour and poor outcome. Lastly, we show that in patients receiving adjuvant chemotherapy (but not targeted anti-HER2 therapy), MYC amplification is associated with a poor outcome in HER2+ breast cancer patients. These findings demonstrate the importance of molecular context in oncogenic transformation and acquisition of a malignant stem-like phenotype and have important diagnostic and therapeutic consequences for the clinical management of HER2+ breast cancer. Gene expression analysis of Her2, Myc, and Her2 + Myc over expression on MCF10A cells, with MCF10A vector control comparison

2013-09-24 | E-GEOD-43730 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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