Gene expression of Ewing tumor cell line SBSR-AKS
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE24806 | GEO | 2011/09/30
SECONDARY ACCESSION(S): PRJNA132301
REPOSITORIES: GEO
Similar Datasets
Project description:Ewing tumor cell line SBSR-AKS grows adherent to the culture vessel. A spontaneously derived sub-line of cell line SBSR-AKS shows growth in suspension. We used microarrays to analyse gene expression in these Ewing tumor cell lines Established Ewing tumor cell lines were grown under standard conditions
2011-09-29 | E-GEOD-24806 | biostudies-arrayexpress
Project description:Gene expression of Ewing tumor cell line SBSR-AKS
| PRJNA132301 | ENA
Project description:<p>Human embryonic kidney 293 (HEK293) cells have been successfully adapted from adherent to suspension culture and have been widely applied in both scientific research and the pharmaceutical industry. However, the alterations in cells during the adaptation have not been well described, which raise some uncertainties and concerns regarding the underlying changes and cell behavior.</p><p>In this work, we adapted adherent HEK293 to suspension culture with desirable cell growth and high production titers for recombinant adenoviral vectors, and cells at several stages throughout the process were characterized. First, we obtained three strains of suspension cells from adherent parental HEK293 cells by gradually phasing out fetal bovine serum in original Dulbecco’s modified essential medium with a simultaneous medium replacement with four serum-free suspension culture media, and one strain was chosen as the preferred candidate for further studies due to its satisfying cell conditions and adenoviral vector productivity. Slower cell growth rate, lower glucose uptake, increased lactate production, weaker cell-surface adhesion, and prolonged S phase in the cell cycle were observed in suspension cells compared to their adherent counterparts. We further performed transcriptomics, proteomics, and metabolomics analysis to identify key switches in cells. A total of 2476 differential genes were found, including 1218 up-regulated genes and 1258 down-regulated genes in suspension cells. A similar and correlated pattern was observed in the proteomic study: an almost balanced up-down regulation between suspension and adherent cells, and 702 differentially expressed metabolites were identified by untargeted metabolomics. By virtue of enrichment analysis on differentially expressed genes, proteins and metabolites, we summarized that HEK293 adherent cells survived and adapted to suspension culture by structural remodelling, metabolic network reconstruction and inherent stress resistance. Additionally, we identified claudin7 as a key player involved in suspension transformation in both transcriptomic and proteomic aspects. Our results provide a molecular enlightenment for the mechanism of suspension adaptation and new directions for the rational design of genetically engineered HEK293-derived cell lines for viral-vectored vaccine production.</p>
2025-12-16 | MTBLS13517 | MetaboLights
Project description:Vero cells, as approved by the World Health Organization, have been the most commonly used continuous cell line for viral vaccine production over the last 25 years, but their adherent phenotype continues to limit productivity. Adapting to a suspension culture would overcome this restriction and reduce production costs. First, a Vero suspension isolate was obtained and metabolically characterized. Second, RNA sequencing analysis was used to identify differentially expressed genes between adherent and suspension cells, which revealed complete downregulation of adhesion and matrix-associated genes. Additionally, signaling pathways involving Wnt and other tyrosine kinase receptors were identified as potential leads for growth optimization. In particular, supplementation with fibroblast growth factor 2 allowed for a 20% increase in cell density. Finally, a comparative viral productivity assay revealed a 30% increase in poliovirus production in suspension Vero cells compared to adherent cells depending on the serotype, as well as a 140% increase in respiratory syncytial virus production and a 150% increase in yellow fever virus production.This work establishes the potential of the suspension Vero cell line as a new cell platform for viral vaccine production.
2024-06-18 | GSE250417 | GEO
Project description:In this work, changes in the proteome level during a step-wise adaptation of an adherent Madin Darby canine kidney (MDCK) cell line to suspension growth and chemically defined medium were analyzed.
2015-04-22 | PXD001306 | Pride
Project description:Ewing sarcoma is an aggressive pediatric small round cell tumor that predominantly occurs in bone. Approximately 85% of Ewing sarcomas harbor the EWS/FLI fusion protein, which arises from a chromosomal translocation, t(11:22)(q24:q12). EWS/FLI interacts with numerous lineage-essential transcription factors to maintain mesenchymal progenitors in an undifferentiated state. We previously showed that EWS/FLI binds the osteogenic transcription factor RUNX2 and prevents osteoblast differentiation. In this study, we investigated the role of another Runt-domain protein, RUNX3, in Ewing sarcoma. RUNX3 participates in mesenchymal-derived bone formation and is a context dependent tumor suppressor and oncogene. RUNX3 was detected in all Ewing sarcoma cells examined, whereas RUNX2 was detected in only 73% of specimens. Like RUNX2, RUNX3 binds to EWS/FLI via its Runt domain. EWS/FLI prevented RUNX3 from activating the transcription of a RUNX-responsive reporter, p6OSE2. Stable suppression of RUNX3 expression in the Ewing sarcoma cell line A673 delayed colony growth in anchorage independent soft agar assays and reversed expression of EWS/FLI-responsive genes. These results demonstrate an important role for RUNX3 in Ewing sarcoma. RNA-seq to compare transcriptiome of control A673 ewing sarcoma cells stably expression a non-target or RUNX3 shRNA
2014-05-01 | E-GEOD-56900 | biostudies-arrayexpress
Project description:RNA-sequencing of PEO1 cells grown in suspension (SUS1 and SUS3) was performed to evaluate transcriptional reprogramming during anokis escape. CRISPR/Cas9 screen of PEO1 cells grown in adherent and suspension culture settings for 5 days or 10 days. GeCKO v2 library transduced in PEO1 cell line and cells were selected with puromycin. PEO1 line was authenticated prior to sequencing. PEO1 parental were confirmed to be BRCA2-mutated (5139C>G).
2018-12-04 | GSE123290 | GEO
Project description:Analysis of differentially expressed genes in wild type A4573 Ewing Sarcoma cells when compared to A4573 Ewing Sarcoma cells that received six 4 Gy fractions (cumulative dose of 24 Gy) of ionizing radiation (radiation-adapted cell line). The hypothesis tested being that repeated ionizing radiation exposure of modifies radiation therapy response in Ewing Sarcoma.
2017-05-10 | GSE98706 | GEO
Project description:Polyamine metabolism and signaling play important roles in multiple cancers including neuroblastoma and breast cancer but have not previously been studied in Ewing sarcoma. Prior work in our lab suggested that tumor microenvironment affects arginase expression -- orthotopically implanted hindlimb tumors with enhanced metastatic potential demonstrate diminished arginase expression compared to subcutaneously implanted tumors that do not metastasize. As arginase catalyzes the conversion of arginine to ornithine, the precursor for polyamine synthesis, this suggested a potential role for polyamine synthesis in Ewing sarcoma metastasis and a target for therapeutic intervention. Here, we show that blocking polyamine synthesis with D, L-alpha-difluoromethylornithine (DFMO) causes a G1 cell cycle arrest, dose-dependent decreases in sarcosphere formation from Ewing sarcoma cell lines growing in non-adherent conditions and a decrease in clonogenic growth in soft agar. Further, we utilized our orthotopic implantation/amputation model of Ewing sarcoma metastasis to investigate the impact of disrupting polyamine synthesis on tumor growth and metastasis. When mice were treated with low dose DFMO, there was no effect on primary tumor growth or metastatic potential; however, at higher concentrations, systemic DFMO slowed primary tumor growth in addition to limiting metastasis. RNA sequencing demonstrated gene expression patterns consistent with induction of ferroptosis caused by polyamine depletion, and this was confirmed experimentally. Collectively, these results reveal a novel mechanism by which DFMO prevents metastasis – induction of ferroptosis due to polyamine depletion, and our results suggest that DFMO may be a readily translatable and well-tolerated treatment to prevent metastatic recurrence in patients with high-risk Ewing sarcoma.
2025-07-16 | GSE274115 | GEO
Project description:We identified slow-cycling cells (SCCs) in Ewing sarcoma using a label retention assay with CFSE. We labeled cells of SK-ES-1, an Ewing sarcoma cell line, with CFSE. After 5 days culture, we isolated cells retaining strong fluorescence (upper, ~10%) as SCCs and other cells (lower, ~90%) as non-slow-cycling cells (non-SCCs) using FACS AriaTM Ⅲ cell sorter.
2022-10-17 | GSE204671 | GEO