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Expression data from U-2 OS osteosarcoma cell lines stably expressing an S22A-progerin mutant compared with U-2 OS expressing wt-progerin

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Mathieu Vernier

PROVIDER: E-GEOD-51349 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from U-2 OS osteosarcoma cell lines stably expressing an S22A-progerin mutant compared with U-2 OS expressing wt-progerin

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

Expression data from H1299 human non-small cell lung carcinoma cell lines stably expressing CHES1 compared with H1299 infected with an empty vector

Project description:The expression of the forkhead transcription factor CHES1, also known as FOXN3, is reduced in many types of cancers. In vitro, CHES1 expression suppresses cell proliferation in tumor cell lines but not in normal cells. Conversely shRNA-mediated depletion of CHES1 increases tumor cell proliferation. We used microarrays to characterize the gene expression changes induced by CHES1 in H1299 cancer cells H1299 cells were infected with a retroviral vector that expresses CHES1 or an empty vector. After 5 days of infection, RNA was extracted from three independent replicas of each condition. Total RNA was send to Genome Quebec service for hybridization with Affymetrix microarrays.

2013-08-01 | E-GEOD-49422 | biostudies-arrayexpress

Expression data from human primary fibroblasts (IMR90) stably expressing H-RasV12 and shRNA against ERK2 or a non-targeting shRNA

Project description:Oncogenic ras activates several signaling pathways that cooperate in cell transformation. They include the ERK/MAP kinase pathway, the PI3K pathway and the Ral pathway among others. Surprisingly, in primary human fibroblasts, oncogenic ras expression induces senescence not transformation, but upon knockdown of ERK2 senescence is bypassed and transformation is stimulated. We used microarrays to characterize the gene expression programme of cells transformed by oncogenic ras, telomerase and knockdown of the ERK2 kinase. Primary human fibroblasts were co-infected with a retroviral vector that expresses oncogenic ras and either a control shRNA or an shRNA against ERK2. Cells with oncogenic ras and shRNA control entered senescence while cells with oncogenic ras and shRNA ERK2 bypassed senescence and underwent malignant transformation. Triplicates of these populations were used to purify total RNA, which we sent to Genome Quebec service for hybridization with Affymetrix microarrays.

2014-10-01 | E-GEOD-33613 | biostudies-arrayexpress

Burkholderia pseudomallei OS strain:OS

Project description:Burkholderia pseudomallei OS strain:OS Genome sequencing and assembly

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Gene expression profile at single cell level of cells from OS tissue of OS lung metastatic patient

Project description:The tumor microenvironment remains unclear in OS lung metastatic patient. We used single cell RNA-seq to analyze the non-immune and immune landscape of the tumor microenvironment in OS patients.

2024-01-17 | GSE234187 | GEO

Progerin-induced changes in gene expression

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

The effect of progerin expression on alternative splicing in keratinocytes of HGPS mice

Project description:Exon level expression analysis for the HGPS pathological aging study data set to analyze the effect of progerin expression on alternative splicing in keratinocytes of HGPS mice. Analysis of the effect of pathological aging (transgenic progerin expression) on alternative splicing (AS) using exon microarrays to interrogate the differential exon usage of the entire genome of HGPS mice (postnatal day 24 and 35) and their wild-type litter mates. Our results suggests that early expression of progerin impairs developmental splicing but that as progerin accumulates, the number of genes with AS increases, similar to what is observed in aging wild-type mice. This dataset is one of the 2 datasets in the overall study. An additional data set series is available with exon expression analysis of aging wild-type mice to analyze the effect of age on alternative splicing during physiological aging. The two datasets are linked together in the SuperSeries GSE67289. A link to the SuperSeries is available at the bottom of this page. 16 skin keratinocyte samples from 2 different age groups: postnatal day 24 and postnatal day 35, from 8 HGPS samples and 8 genotype negative (wild-type) littermates.

2015-11-01 | E-GEOD-67288 | biostudies-arrayexpress

Progerin Expression in Endothelial Cells Induces Endothelial Dysfunction

Project description:Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare, genetic premature aging disorder associated with severe atherosclerosis, often resulting in fatal heart attacks and strokes. Progerin, the mutant protein in HGPS, also is expressed in healthy individuals and may play a role in the development of atherosclerosis during physiologic aging. Here, we provide evidence for a primary involvement of vascular endothelium in the pathogenesis of accelerated atherosclerosis in HGPS. Expression of progerin in cultured human endothelial cells induces a dysfunctional phenotype, manifested by activation of multiple pro-inflammatory, pro-atherogenic genes. In particular, our data implicate endothelial-derived interleukin-1 (IL-1) as a key mediator of a pro-inflammatory vascular phenotype. Endothelial activation also is detectable in a mouse model of HGPS, and appears to be conveyed to neighboring vascular cells via autocrine and paracrine signaling. These new mechanistic insights into the vascular pathobiology of HGPS may have therapeutic implications for this disease. Genome-wide transcriptional profiling was carried out to assess functional phenotypic changes in endothelial cells (EC) as a result of progerin expression. Cultured EC were infected with an adenovirus expressing progerin (Ad-Progerin), and as a control, an adenovirus that did not express any construct (Ad-Null). Experiments were preformed with three different EC cultures.

2010-12-02 | E-GEOD-19270 | biostudies-arrayexpress

RNA-seq analysis after STXBP5 overexpression or STXBP5 knockdown in HA-progerin HEK293 cells

Project description:Hutchinson-Gilford Progeria Syndrome (HGPS) is caused by a mutant LMNA called progerin. To determine the mechanism of STXBP5 on progerin, we over expressed STXBP5 or knocked down STXBP5 in HA-progerin HEK293 cells, then analyzed the effect on the expression of coding genes. In this study, we identified STXBP5 as an influencing factor for HA-progerin HEK293 cells. Lowering the expression of STXBP5 may be a new therapeutic strategy for treating age-related phenotypes in HGPS.

2024-09-14 | GSE243095 | GEO

Gene expression profile of U2-OS control and NSD3 knockdown cells

Project description:Osteosarcomas (OS) have highly chaotic genomes, yet their cancer drivers are poorly defined. Leveraging cross-species OS genomics we identify the frequent amplification of NSD3, a histone lysine methyltransferase and expose the NSD3-ARID3A axis as a core pathway in osteosarcomagenesis. Loss- and gain-of-function studies with CRISPR-Cas9 and lentivirus systems establish the causal role of NSD3 in OS tumor growth and spontaneous metastasis.

2021-08-03 | GSE118129 | GEO

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