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Gene expression profiles of ovarian cancer cells by inhibiting Hh signaling

ABSTRACT: Analysis of gene expression levels in response to inhibition of Hh signaling in ovarian cancer cells using a cDNA microarray technique. Results suggest that 208 genes (50.5%) were up-regulated and 204 gene (49.5%) were down-regulated after GANT61 treatment.The focal adhesion and ECM-receptor interaction cross-talk in SKOV3 cells after treatment with GANT61, and the expression change of “focal adhesion” related genes play an important role in the processes of response to GANT61-treatment. SKOV3 cells were treated with GANT61 (20 μM for 60 hr) and control vehicle DMSO, respectively.

ORGANISM(S): Homo sapiens

SUBMITTER: Shiwen Luo

PROVIDER: E-GEOD-53464 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression profiles of ovarian cancer cells by inhibiting Hh signaling

Project description:Analysis of gene expression levels in response to inhibition of Hh signaling in ovarian cancer cells using a cDNA microarray technique. Results suggest that 208 genes (50.5%) were up-regulated and 204 gene (49.5%) were down-regulated after GANT61 treatment.The focal adhesion and ECM-receptor interaction cross-talk in SKOV3 cells after treatment with GANT61, and the expression change of “focal adhesion” related genes play an important role in the processes of response to GANT61-treatment.

2014-01-15 | GSE53464 | GEO

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

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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.

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RNA-seq of human ovarian cancer cell line SKOV3 treated with BMP2 against untreated controls

Project description:To elucidate the biological function of BMP2 in ovarian cancer cells, SKOV3, a human ovarian cancer cell line, was stimulated with BMP2.

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RNA-seq of human ovarian adenocarcinoma cell line SKOV3 treated with bisphenol A (10 or 100 nM) against untreated controls

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

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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

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Gene expression change in Skov3 after EZH2 knockdown

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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

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Transcriptional profiling of glucose deprivation resistant and glucose deprivation sensitive clones derived from IGROV-1 and SKOV3 ovarian cancer models and cultivated under either normal-glucose or low-glucose condition

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