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

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

ORGANISM(S): Mus musculus

SUBMITTER: Alistair Chalk

PROVIDER: E-GEOD-47572 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

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

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

PTHR1 knock-down in osteosarcoma cells

Project description: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

2015-07-01 | E-GEOD-46861 | biostudies-arrayexpress

Overexpression of cSki in hematopoietic stem and progenitor cells

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Modeling tumor subtypes in vivo using lineage restricted transgenic shRNA

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

Oxidoreductase transcript data from human umbilical vein endothelial cells

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Expression data from 26972c yeast M-BM-1 bHLHm1 (SAT1)

Project description:26972c yeast cells were transformed with either empty vector (pYES3) or pYES3:Gm:bHLHm1. Cells were grown on low ammonium concentrations to observe transcriptional changes in the yeast genome in response to the soybean bHLHm1 transcription factor. The ammonium transport mutant (26972c) was transformed with either a empty vector control (pYES3) or pYES3 containing GmbHLHm1.Independent replicates (3) for each treatment were grown for 12 hours in the presence of 1 mM ammonium and 2 % w/vol galactose to activate the Gal promoter located on pYES3. Cells were harvested and total RNA extracted. Quantified RNA was analaysed using microarray analysis using the [Yeast_2] Affymetrix Yeast Genome 2.0 Array.

2014-03-12 | E-GEOD-55804 | 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

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