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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Robert Strauss

PROVIDER: E-GEOD-15351 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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 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

Resistance of primary ovarian cancer cells to oncolytic adenoviruses

Project description: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

2009-04-01 | E-GEOD-15473 | biostudies-arrayexpress

Differential gene expression profiles between SKOV3.ip1-S116A cells (Ser116 of PEA-15 substituted with alanine) and SKOV3.ip1-S116D cells (Ser116 of PEA-15 substituted with aspartic acid).

Project description:To dissect the molecular mechanisms of PEA-15-mediated paclitaxel sensitization in ovarian cancer cells, we performed cDNA microarray analysis using SKOV3.ip1-S116A cells (Ser116 of PEA-15 substituted with alanine) and SKOV3.ip1-S116D cells (Ser116 of PEA-15 substituted with aspartic acid). cDNA microarray data analysis showed that SCLIP (SCG10-like protein), also known as STMN3, was highly expressed in SKOV3.ip1-S116D cells and was involved in pPEA-15-mediated paclitaxel sensitization in ovarian cancer cells. SKOV3.ip1-S116A cells (Ser116 of PEA-15 substituted with alanine) and SKOV3.ip1-S116D cells (Ser116 of PEA-15 substituted with aspartic acid) were used. Total RNA was extracted and purified using RNeasy mini kit (Qiagen, Inc.) according to the manufacturerM-bM-^@M-^Ys instructions. The integrity of the obtained RNA was assessed using an Agilent 2100 BioAnalyzer (Agilent Technologies). The Affymetrix HGU133 plus platform was used for hybridization, staining, and imaging of the arrays by following the manufacturerM-bM-^@M-^Ys instructions. Gene expression analysis was performed in triplicate.

2012-05-11 | E-GEOD-37934 | biostudies-arrayexpress

Differential gene expression profiles between SKOV3.ip1-S116A cells (Ser116 of PEA-15 substituted with alanine) and SKOV3.ip1-S116D cells (Ser116 of PEA-15 substituted with aspartic acid).

2012-05-12 | GSE37934 | GEO

Differential gene expression in ovarian cancer cell lines treated with vehicle or norepinephrine

Project description:Gene expression profiling was carried out HeyA8 and SKOV3-ip1 ovarian cancer cell lines, treated either with vehicle control or 10 uM norepinephrine. The primary research question is whether ovarian cancer cell gene expression differs as a function of norepinephrine exposure. Gene expression profiling was carried out HeyA8 and SKOV3-ip1 ovarian cancer cell lines, treated either with vehicle control or 10 uM norepinephrine.

2011-12-14 | E-GEOD-34405 | biostudies-arrayexpress

Differential gene expression in ovarian cancer cell lines treated with vehicle or norepinephrine

2011-12-14 | GSE34405 | GEO

Gene expression of SKOV3 cells after no treatment or treatment with 50 microM peracetylated GlcNAc or peracetylated 4-deoxy-GlcNAc for three days

Project description:Heparan sulfate (HS), a long linear polysaccharide, is implicated in various steps of tumorigenesis, including angiogenesis. We successfully interfered with HS biosynthesis using a peracetylated 4-deoxy analog of the HS constituent GlcNAc and studied the compoundM-bM-^@M-^Ys metabolic fate and its effect on angiogenesis. The 4-deoxy analog was activated intracellularly into UDP-4-deoxy-GlcNAc and HS expression was inhibited up to ~96% (IC50 = 16 M-BM-5M). HS chain size was reduced, without detectable incorporation of the 4-deoxy analog, likely due to reduced levels of UDP-GlcNAc and/or inhibition of glycosyltransferase activity. Comprehensive gene expression analysis revealed reduced expression of genes regulated by HS binding growth factors as FGF-2 and VEGF. Cellular binding and signaling of these angiogenic factors was inhibited. Micro-injection in zebrafish embryos strongly reduced HS biosynthesis, and angiogenesis was inhibited in both zebrafish and chicken model systems. All these data identify 4-deoxy-GlcNAc as a potent inhibitor of HS synthesis which hampers pro-angiogenic signaling and neo-vessel formation. 9 samples were analyzed: 3 biological replicates from untreated SKOV3 cells, 3 biological replicates from SKOV3 cells treated with peracetylated GlcNAc, 3 biological replicates from SKOV3 cells treated with peracetylated 4-deoxy-GlcNAc

2013-08-23 | E-GEOD-48284 | biostudies-arrayexpress

Gene expression change in Skov3 after EZH2 knockdown

Project description:To identify genes whose expression was suppressed by EZH2, we performed gene expression microarray analysis in control and EZH2 knockdown human SKOV3 EOC cells. Two individual short hairpin RNAs to the human EZH2 gene (shEZH2) were used to limit potential off-target effects. Two individual short hairpin RNAs to the human EZH2 gene (shEZH2) were used to limit potential off-target effects. Three technical replicates per group were used.

2011-12-12 | E-GEOD-31433 | biostudies-arrayexpress

Gene expression profile of SKOV3 cells cultured with a novel 3D cell culture method

Project description:Preclinical cancer drug discovery efforts have employed two-dimensional (2D)-cell-based assay models, which fail to forecast in vivo efficacy and contribute to a lower success rates of clinical approval. Three-dimensional (3D) cell culture models are recently expected to bridge the gap between 2D and in vivo models. We have developed a novel 3D culture method that improves the growth of spheroid-forming cancer cells under anchorage-independent condition by leveraging a feature of FP001, a bacteria-derived polysaccharide. Gene microarrays were used to observe the global gene expression in SKOV3 cells cultured with adhesion condition (2D, control) or with low adhesion condition (FP001) and identified distinct classes of up or down-regulated genes. SKOV3 cells were cultured for 11 days in normal attachment plates with normal medium (as control) or low-attachment plates with FP001 containing medium. Each sample was collected three times.

2015-07-31 | E-GEOD-69523 | 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

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