Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA222797 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To determine the molecular basis for CD99 function in osteosarcoma, gene expression profile of U-2/CD99 wild-type(wt) expressing cell lines were compared with U-2 OS parental cells.
2014-06-29 | GSE39072 | GEO
Project description:Disassembly of the nuclear envelope is an essential feature of mammalian cell division controlled by the phosphoryaltion of lamins via cyclin dependent kinases. This process is affected in cells expressing progerin, a lamin A allele found in patients with Hutchinson-Gilford Progeria syndrome. Progerin can inhibit cell proliferation of both normal and tumor cells and this property is largely magnified if its phosphorylation at serine 22 is inhibited by a genetic mutation to generate S22A-progerin. Surprisingly, S22A-progerin acquires the ability to trigger cellular senescence in tumor cells with mutations in the p53 and RB tumor suppression pathways suggesting a novel pathway to control the growth of malignant tumors. We used microarrays to characterize the gene expression changes induced by the S22A-progerin in comparison with the wt-progerin in U-2 OS cell line. U-2 OS cells were infected with a retroviral vector that express S22A-progerin or wt-progerin. After 4 days of infection, RNA was extracted from three independents replicas of each condition. Total RNA was send to Genome Quebec service for hybridization with Affymetrix microarrays.
2014-03-01 | E-GEOD-51349 | biostudies-arrayexpress
Project description:expression analysis from a genetically engineered mouse model of osteosarcoma; determine the expression profile of mouse osteosarcoma Experiment Overall Design: 3 control in vitro differentiated WT primary osteoblasts; 15 primary osteosarcoma; 4 OS cell lines; 4 secondary tumours
2008-10-20 | E-GEOD-9460 | biostudies-arrayexpress
Project description:Disassembly of the nuclear envelope is an essential feature of mammalian cell division controlled by the phosphoryaltion of lamins via cyclin dependent kinases. This process is affected in cells expressing progerin, a lamin A allele found in patients with Hutchinson-Gilford Progeria syndrome. Progerin can inhibit cell proliferation of both normal and tumor cells and this property is largely magnified if its phosphorylation at serine 22 is inhibited by a genetic mutation to generate S22A-progerin. Surprisingly, S22A-progerin acquires the ability to trigger cellular senescence in tumor cells with mutations in the p53 and RB tumor suppression pathways suggesting a novel pathway to control the growth of malignant tumors. We used microarrays to characterize the gene expression changes induced by the S22A-progerin in comparison with the wt-progerin in U-2 OS cell line.
2014-03-01 | GSE51349 | GEO
Project description:Osteosarcoma (OS) is a common primary bone malignancy that is characterized by high degree of aneuploidy, gene amplification, and multiple unbalanced chromosomal rearrangements. The human osteosarcoma U-2 OS and Sa OS cells lines have been generated more than three decades ago and are used in a wide spectrum of biomedical research. Nevertheless, and despite scattered information about their genetic context, no comprehensive comparative study of their transcriptome profile has been reported to date. The aim of this study was to elucidate common molecular characteristics of the two cell lines as well as differences in their expression profile. Thus the genome wide gene expression profile of the Sa OS cells was compared with reference RNA of U-2 OS cells. These results may provide the basis for future studies and illuminate the molecular differences of the two widely used cell lines.
2009-09-21 | E-MEXP-1897 | biostudies-arrayexpress
Project description:The premature aging disease Hutchinson-Gilford Progeria Syndrome (HGPS) is caused by constitutive production of progerin, a mutant form of the nuclear architectural protein lamin A1. Progerin is also sporadically expressed in wild type cells and has been linked to physiological aging. HGPS cells exhibit extensive nuclear defects including abnormal chromatin structure and increased DNA damage. At the organismal level, HGPS affects several tissues particularly of mesenchymal origin. How the cellular defects of HGPS cells lead to the organismal defects has been unclear. To begin to unravel how progerin leads to disease phenotypes, we analyzed time-dependent changes in transcriptional profiles in response to progerin expression in a hTERT-immortalized skin fibroblast cell line expressing either GFP-progerin or the GFP-wt lamin A control Keywords: time course, cell line comparison
2008-02-09 | GSE10123 | GEO
Project description:Although the introduction of combined neoadjuvant chemotherapy has significantly prolonged the survival, the outcome of OS patients with poor response to chemotherapy is still unfavorable. To develop new therapeutics the elucidation of the entire molecular pathway regulating OS cell proliferation is warranted. We analysed the expression levels of 933 miRNA probes in surgical 24 samples and 8 cell lines of osteosarcoma with 3D-Gene human miRNA oligo chips. Total RNA was extracted from 24 fresh frozen tumour specimens and 8 OS cell lines. We analysed the global miRNA exprssion profiles of these osteosarcoma cases in order to find new novel potential targets for the development of therapeutic targeting OS.
2012-09-01 | E-GEOD-30934 | biostudies-arrayexpress
Project description:Gene expression of T47D-MTVL human breast cancer cells expressing Dox-inducible shRNAs against histone H1.4 (sh120) or multiple H1 variants (sh225), or overexpressing WT or K26A mutant HA-tagged H1.4. T47D-MTVL, breast cancer cell line carrying one stably integrated copy of luciferase reporter gene driven by the MMTV promoter, is stably infected with an inducible system for the expression of shRNAs.Cells stably express RedFP and KRAB repressor fused to Tet regulator.Upon Dox treatment, cells express RedFP and the cloned shRNA. Stable breast cancer-derived cell lines expressing an shRNA against one of each of the histone H1 isoforms in response to doxycycline (Dox) were grown for six days in the presence or absence of Dox, in duplicate, and RNA extracted for microarray hybridization. Cell lines used: inducible shRNA against H1.4 or multiple H1 variants, and random shRNA-expression vector. Stable breast cancer-derived cell lines expressing the histone H1.4 isoform, WT or K26A, HA-tagged, in duplicate, and RNA extracted for microarray hybridization. Cell lines used: overexpressing H1.4 WT or K26A mutant.
2014-05-16 | E-GEOD-55786 | biostudies-arrayexpress
Project description:miRNA Expression data from human osteosarcoma (OS)
| PRJNA288576 | ENA