Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Resistance of primary ovarian cancer cells to oncolytic adenoviruses

ABSTRACT: This SuperSeries is composed of the following subset Series: GSE15350: Resistance of primary ovarian cancer cells to oncolytic adenoviruses part1 of 2 GSE15351: Resistance of primary ovarian cancer cells to oncolytic adenoviruses part2 of 2 Refer to individual Series

ORGANISM(S): Homo sapiens

SUBMITTER: Robert Strauss

PROVIDER: E-GEOD-15473 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Epithelial phenotype confers resistance of ovarian cancer cells to oncolytic adenoviruses.

Strauss Robert R Sova Pavel P Liu Ying Y Li Zong Yi ZY Tuve Sebastian S Pritchard David D Brinkkoetter Paul P Möller Thomas T Wildner Oliver O Pesonen Sari S Hemminki Akseli A Urban Nicole N Drescher Charles C Lieber André A

Cancer research 20090602 12

We studied the susceptibility of primary ovarian cancer cells to oncolytic adenoviruses. Using gene expression profiling of cancer cells either resistant or susceptible to viral oncolysis, we discovered that the epithelial phenotype of ovarian cancer represents a barrier to infection by commonly used oncolytic adenoviruses targeted to coxsackie-adenovirus receptor or CD46. Specifically, we found that these adenovirus receptors were trapped in tight junctions and not accessible for virus binding. ...[more]

PMID: 19491256

Similar Datasets

Resistance of primary ovarian cancer cells to oncolytic adenoviruses part2 of 2

Project description:The mechanisms of primary ovarian cancer cells for resistance to viral oncolysis were investigated using Ad5/35.IR.E1A/TRAIL on clonal cultures derived from ovc316m cells. Part 2 of 2, 26 clonal ovc316m cultures additionally to Resistance of primary ovarian cancer cells to oncolytic adenoviruses part1 of 2 Cells were infected for 8 days and cell survival determined by MTT assay. Uninfected control cells of each clonal culture were utilized for DNA expression arrays. SKOV3-ip1 cells were used for reference RNA in all samples. The reference RNA from SKOV3-ip1 cells for part 2 of 2 had to be re-amplified.

2009-04-01 | E-GEOD-15351 | biostudies-arrayexpress

Resistance of primary ovarian cancer cells to oncolytic adenoviruses part1 of 2

Project description:The mechanisms of primary ovarian cancer cells for resistance to viral oncolysis were investigated using Ad5/35.IR.E1A/TRAIL on clonal cultures derived from ovc316m cells. Part 1 of 2, initital study involving 5 clonal ovc316m cultures Cells were infected for 8 days and cell survival determined by MTT assay. Uninfected control cells of each clonal culture were utilized for DNA expression arrays. SKOV3-ip1 cells were used for reference RNA in all samples.

2010-06-20 | E-GEOD-15350 | biostudies-arrayexpress

Paclitaxel resistance in ovarian cancer increases oncolytic adenovirus efficacy via upregulated CAR expression and dysfunctional cell cycle control

Project description:The microtubule-stabilising drug paclitaxel has activity in relapsed ovarian cancer. However, resistance frequently develops. Oncolytic adenoviruses are a novel cancer therapy, and replicate selectively within and lyse malignant cells, leading to productive infection of neighbouring cells. We found increased efficacy of adenoviruses of multiple subtypes in paclitaxel-resistant ovarian cancer cells. There was increased expression of a key adenovirus receptor, CAR (coxsackie adenovirus receptor), due to increased transcription that resulted from histone modification. Moreover, CAR transcription increased in intraperitoneal xenografts with acquired paclitaxel resistance and in tumours from patients with paclitaxel-resistant ovarian cancer. Finally, we identified dysregulated cell cycle control as a second mechanism of increased adenovirus efficacy in paclitaxel-resistant ovarian cancer and that inhibition of CDK4/6 using PD-0332991 was able both to reverse paclitaxel resistance and reduce adenovirus efficacy. Thus, paclitaxel resistance increases oncolytic adenovirus efficacy via at least two separate mechanisms. Parental SKOV3 and paclitaxel-resistant SKOV3-TR cells were analysed in duplicate

2015-12-10 | E-GEOD-54772 | biostudies-arrayexpress

Discovery of Tamoxifen and N-Desmethyl Tamoxifen Protein Targets in MCF-7 Cells Using Large-Scale Protein Folding and Stability Measurements

Project description:The proteins in an MCF-7 cell line were probed for tamoxifen (TAM) and n-desmethyl tamoxifen (NDT) induced stability changes using the Stability of Proteins from Rates of Oxidation (SPROX) technique in combination with two different quantitative proteomics strategies. Together the SILAC- and iTRAQ-SPROX experiments described here enabled over 1000 proteins to be assayed for TAM- and NDT- induced protein stability changes, and a total of 163 and 200 protein hits were identified in the TAM and NDT studies, respectively. A subset of high confidence hits were assessed for experimental links to the ER using a STRING analysis. TAM was shown to induce stabilization of Y-box binding protein 1 (YBX1), a protein recently shown to bind the estrogen receptor. TAM was shown to directly interact with purified recombinant YBX1 with Pulse Proteolysis (PP). These results support YBX1 as a direct protein target of TAM. Proteins with altered expression levels with TAM and NDT treatment were identified with SILAC quantitation. In total, 799 and 671 proteins were probed for TAM- and NDT- induced expression changes, respectively, and 49 and 30 proteins had altered expression. This work also involved the use of a novel data analysis strategy to identify protein targets of ligands using the SPROX technique.

2019-11-08 | PXD006732 | Pride

Gene Expression analysis of hESC B2M knock-out

Project description:The clinical use of human pluripotent stem cells and their derivatives is limited by the rejection of transplanted cells due to differences in their HLA genes. This has led to the proposed use of histocompatible, patient-specific stem cells, however the preparation of many different stem cell lines for clinical use is a daunting task. Here we develop two distinct genetic engineering approaches that address this problem. First, we use a combination of gene targeting and mitotic recombination to derive HLA-homozygous embryonic stem cell (ESC) subclones from an HLA-heterozygous parental line. A small bank of HLA-homozygous stem cells with common haplotypes would match a significant proportion of the population. Second, we derive HLA class I-negative cells by targeted disruption of both alleles of the B2M gene in ESCs. Mixed leukocyte reactions and peptide-specific HLA-restricted CD8+ T cell responses were reduced in class I-negative cells that had undergone differentiation in embryoid bodies. These B2M-/- ESCs could act as universal donor cells in applications where the transplanted cells do not express HLA class II genes. Both approaches used adeno-associated virus (AAV) vectors for efficient gene targeting in the absence of potentially genotoxic nucleases, and produced pluripotent, transgene-free cell lines. Total RNA, 4 samples were analyzed as follows: 2 replicates for the hESC H1 wt ( rep1 and rep2) and 2 independent clones of hESC B2M knock-out

2014-01-01 | E-GEOD-42289 | biostudies-arrayexpress

A genome-wide analysis reveals that the Drosophila transcription factor, Lola, promotes axon growth in part by suppressing expression of the actin nucleation factor, Spire (allele lola_ORE76)

Project description:Transcriptional profiling of Drosophila embryos comparing lola mutant 10-12 hour after egg lay (AEL) embryos to age-matched control embryos. Mutants are homozygous lola nulls (allele lola_ORE76). Two-condition experiment: lola mutant embryos vs. age-matched control embryos. 7 biological replicates, each sample independently collected and containing RNA from approximately 300 embryos. Mutant and control embryos for each replicate were collected simultaneously. Dye-swaps were performed.

2011-12-03 | E-GEOD-34121 | biostudies-arrayexpress

A genome-wide analysis reveals that the Drosophila transcription factor, Lola, promotes axon growth in part by suppressing expression of the actin nucleation factor, Spire (allele lola_ORC4)

Project description:Transcriptional profiling of Drosophila embryos comparing lola mutant 10-12 hour after egg lay (AEL) embryos to age-matched control embryos. Mutants are homozygous isoform K nulls (allele lola_ORC4). Two-condition experiment: lola mutant embryos vs. age-matched control embryos. 7 biological replicates, each sample independently collected and containing RNA from approximately 300 embryos. Mutant and control embryos for each replicate were collected simultaneously. Dye-swaps were performed.

2011-12-03 | E-GEOD-34122 | biostudies-arrayexpress

A genome-wide analysis reveals that the Drosophila transcription factor, Lola, promotes axon growth in part by suppressing expression of the actin nucleation factor, Spire

Project description:This SuperSeries is composed of the following subset Series: GSE34121: A genome-wide analysis reveals that the Drosophila transcription factor, Lola, promotes axon growth in part by suppressing expression of the actin nucleation factor, Spire (allele lola_ORE76) GSE34122: A genome-wide analysis reveals that the Drosophila transcription factor, Lola, promotes axon growth in part by suppressing expression of the actin nucleation factor, Spire (allele lola_ORC4) Refer to individual Series

2011-12-03 | E-GEOD-34123 | biostudies-arrayexpress

Thymosin α1 reverses oncolytic adenovirus-induced M2 polarization of macrophages to improve antitumor immunity and therapeutic efficacy

Project description:Although oncolytic adenoviruses have been widely studied for their direct oncolytic activity and immunomodulatory role in cancer immunotherapy, the immunosuppressive feedback loop induced by oncolytic adenoviruses remains poorly studied. Here, we showed that type V adenovirus (ADV) induces the polarization of tumor-associated macrophages (TAMs) to the M2 phenotype and increases the infiltration of regulatory T cells (Tregs) in the tumor microenvironment (TME). By selectively compensating for these deficiencies, Tα1 reprogrammed “M2-like” TAMs toward an antitumoral phenotype, thereby reprogramming the TME into a state more beneficial for antitumor immunity. Moreover, ADVTα1 was constructed by harnessing the merits of all the components for the aforementioned combinatorial therapy. Both in vitro and in vivo data showed that both exogenously supplied and adenovirus-produced Tα1 orchestrate TAM reprogramming and enhance the antitumor efficacy of ADV via CD8+ T cells, showing promising prospects for clinical translation. Our findings provide inspiration for improving oncolytic adenovirus combination therapy and designing new oncolytic engineered adenoviruses.

2024-06-28 | GSE271046 | GEO

Thymosin α1 reverses oncolytic adenovirus-induced M2 polarization of macrophages to improve antitumor immunity and therapeutic efficacy

2024-07-04 | GSE271202 | GEO