OVCAR-3 Cells: Control vs. FBA-TPQ treated
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: hui wang
PROVIDER: E-GEOD-25317 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Transcriptional profiling of human ovarian cancer cells comparing control vehicle-treated A2780 and OVCAR-3 (Human ovarian cancer cell lines) cells with A2780 and OVCAR-3 cells treated with 5μM LS-98 for 24 hours.Goal was to determine the effects of LS-98 compound on the global A2780 and OVCAR-3 cells gene expression. One-condition experiment, control vehicle-treated A2780 and OVCAR-3 vs. LS098 treated-A2780 and OVCAR-3 cells. Biological replicates: 2 replicates.
2011-06-01 | E-GEOD-29668 | biostudies-arrayexpress
Project description:The purpose of the study was to identify mRNA bound to HuR in the presence of doxorubicin in MCF7 cells. We collected cytoplasmic RNA from untreated and treated cells and detected differentially expressed genes (DEGs). We also coimmunoprecipitated HuR and IgG (as control) from doxorubicin treated cells. Comparison between HuR RIP and IgG RIP signals was used to discriminate specific mRNA bound to HuR. HuR coimmmunoprecipitated material was hybridized together with cytoplasmic mRNA of doxorubicin treated cells, enabling the fold enrichment calculation and the selection of mRNAs bound to HuR. Keywords: RIP-Chip, HuR, doxorubicin, MCF7, HuR consensus binding, post-transcriptional regulation. We subjected MCF7 cells to starvation for 24h and then we added doxorubicin at final concentration of 10 uM, profiling before and after 4 hours of treatment in biological quadruplicate (only on cytoplasmic mRNAs, as HuR was found in the cytoplasm). Differentially expressed genes, altered during the treatment, were identified. Data derived from HuR RIP-Chip and IgG RIP-Chip (in biological quadruplicate) allowed the identification of specific mRNAs bound to HuR. The comparison between HuR RIP-Chip and cytoplasmic extracts from doxorubicin treated cells (in biological triplicate) identified those genes that were more strictly bound to HuR independently from their expression levels.
2011-12-31 | E-GEOD-33055 | biostudies-arrayexpress
Project description:Ovarian cancer is a deadly gynecological malignancy for which novel biomarkers and therapeutic targets are imperative for improving survival. To investigate the role of histone H1 in ovarian cancer cells, we overexpress a histone H1 variant, H1.3, in the OVCAR-3 epithelial ovarian cancer cell line. RNA was extracted from OV-3/H1.3(H) cells (OVCAR-3 with overexpression of H1.3) and control cells of OVCAR-3 transfected with vectors without H1.3. The microarray chip used was human Affymetrix ST1.0 array. Gene expression changes caused by overexpression of H1.3 in OVCAR-3 cells were identified. Affymetrix Human Exon 1.0 ST array was used to identify the changes in transcriptome of OVCAR-3 caused by overexpression of H1.3
2014-10-31 | E-GEOD-61692 | biostudies-arrayexpress
Project description:The androgen receptor (AR) plays a key role in progression to incurable androgen-ablation resistant prostate cancer (PCA). We have identified three novel AR splice variants lacking the ligand binding domain (designated as AR3, AR4 and AR5) in hormone insensitive PCA cells. AR3, one of the major splice variants expressed in human prostate tissues, is constitutively active and its transcriptional activity is not regulated by androgens or antiandrogens. Immunohistochemistry analysis on tissue microarrays containing 429 human prostate tissue samples shows that AR3 is significantly upregulated during PCA progression and AR3 expression level is correlated with the risk of tumor recurrence after radical prostatectomy. Overexpression of AR3 confers ablation-independent growth of PCA cells while specific knock-down of AR3 expression (without altering AR level) in hormone resistant PCA cells attenuates their growth under androgen-depleted conditions in both cell culture and xenograft models, suggesting an indispensable role of AR3 in ablation-independent growth of PCA cells. Furthermore, AR3 may play a distinct yet essential role in ablation-independent growth through regulating a unique set of genes including AKT1, which are not regulated by the prototype AR. Our data suggest that aberrant expression of AR splice variants may be a novel mechanism underlying ablation-independence during PCA progression and AR3 may serve as a prognostic marker to predict patient outcome in response to hormonal therapy. Given that these novel AR splice variants are not inhibited by currently available anti-androgen drugs, development of new drugs targeting these AR isoforms may potentially be effective for treatment of ablation-resistant PCA. Total RNA was extracted from CWR-R1 and 22Rv1 cells treated with shAR3-1, shARa and the scrambled shRNA control, respectively. Each of CWR-R1 and 22Rv1 cells treated with shAR3-1 was compared with the scrambled shRNA control. The same experiments were performed for the cells treated with shARa.
2009-03-16 | E-GEOD-13919 | biostudies-arrayexpress
Project description:Analysis of the ovarian cancer cell line OVCAR-5. A standard trypsin digest was carried out on the OVCAR-5 cell lysates which were then analysed in the un-fractionated and fractionated forms. Fractionation was completed using a peptide IEF separation method. All samples were analysed by nano-LC-ESI-MS/MS using a QTOF.
2016-09-27 | PXD003547 | Pride
Project description:Claudins are tight junction proteins that are involved in tight junction formation and function. Previous studies have shown that claudin-7 is frequently upregulated in epithelial ovarian cancer (EOC) along with claudin-3 and claudin-4. Here, we investigate in detail the expression patterns of claudin-7, as well as its possible functions in EOC. Initially a total of 95 ovarian tissue samples (7 normal ovarian tissues, 65 serous carcinomas, 11 clear cell carcinomas, 8 endometrioid carcinomas and 4 mucinous carcinomas) were studied for claudin-7 expression using RT-PCR analysis. The gene for claudin-7, CLDN7, was found to be significantly upregulated in all the tumor tissue samples studied. Similarly, immunohistochemical analysis and western blotting showed that claudin-7 protein was significantly overexpressed in the vast majority of EOCs. Two cell lines(OVCAR-2 and OVCA420) were chosen for microarray based gene expression analysis using small interfering RNA-mediated(SiRNA) knockdown of claudin-7. This treatment led to significant changes in gene expression that was validated by RT-PCR and immunoblotting. Ovarian cancer lines OVCA420 and OVCAR-2 were cultured in duplicate in McCoy’s 5A growth medium (Invitrogen) supplemented with 10% fetal bovine serum (FBS) and antibiotics (100 units/ml penicillin and 100 mg/ml streptomycin). Cells cultured in 6-well plates were transfected with either Claudin-7 specific siRNA oligos duplexes (Ambion, Inc.Austin, TX) or control siRNA #1 (Dharmacon) using LipofectAMINE 2000 (Invitrogen). Cells were treated for 72 hours to allow maximum knockdown, after which they were harvested for RNA preparation. Total RNA, was extracted using Trizol, quality and quantity were checked using the Agilent 2100 Bioanalyzer with RNA 6000 Nano chip, (Agilent Technologies UK Ltd, West Lothian, UK). Biotinylated cRNA was generated using the Illumina TotalPrep RNA Amplification Kit (Ambion; Austin, TX) starting with approximately 500 ng total RNA. Hybridization of the cRNA was to the Sentrix HumanRef-8 Expression BeadChip (Illumina, Inc., San Diego, CA). Microarray data processing and analysis was performed using Illumina Bead Studio software. Hierarchical clustering analysis of the significant genes was done using the JMP 6.0.0 software. Validation of the expression patterns of selected genes was performed using RT-PCR.
2012-09-19 | E-GEOD-26055 | biostudies-arrayexpress
Project description:Total RNA was extracted using TRIzol from PEO4 and OVCAR-3 cells treated for 72 hours with 10uM GSK6853 or DMSO as a control. In case of BRPF1 silencing experiment, RNA extraction was performed from cells transfected with BRPF-targeting siRNA or nontarget (scramble) siRNA 96 hours post-transfection using TRIzol and Zymo RNA Clean & Concentrator-5 columns. Indexed libraries were prepared starting from 1000 ng of total RNA according to Illumina Stranded Total RNA prep Ligation with Ribo-Zero Plus kit. Final libraries were sequenced at a concentration of 0,6 pM/lane on the Illumina Novaseq 6000 using S4 flowcell and v1.5 reagents. The current study was focused on the investigation of molecular mechanisms underlying the antiproliferative effect of BRPF1 inhibition or silencing in ovarian cancer. To this end, transcriptome changes induced by GSK6853 treatment in chemotherapy-resistant PEO4 and OVCAR-3 cells and BRPF1 silencing in OVCAR-3 cells were analysed.
2024-01-08 | E-MTAB-13663 | biostudies-arrayexpress
Project description:Cotton fiber is actually unicellular trichome, therefor its length is really hard to be modified but very meaningful to fiber quality and yield. We have reported the function of the second RRM domain of Oryza sativa FCA in rice cell size regulation. Data shows it is highly conserved across dicotyledonous and monocotyledonous plants. Here we provide evidence showing that the second RRM domain of Brassica napus FCA worked in Gossypium hirsutum, leading to the enlargement of multiple types of cells, such as pollen, cotyledon petiole and cotton fiber. In the transgenic cotton, the length of unicellular cotton fiber increased by about 10% and fiber yield per plant also showed a dramatic increase, ranging from 35% to 66%, over the control. Thus, this RRM domain may be an ancient and common cell size regulator and has great economic value on cotton industry. FCA encodes a strong promoter of the transition to flowering in Arabidopsis thaliana, which contains two RRM (RNA recognition motif) domain and a WW protein interaction domain (Macknight et al., 1997). We have previously found that cell size and yield of rice (Oryza sativa) can be increased by ectopic expression of the first RRM domain of OsFCA (Hong et al., 2007). The second RRM domain of OsFCA can also increase cell size (Attia et al., 2005), suggesting OsFCA-RRMs each play a role in homeostatic cell size regulation. We designate them as Oryza sativa cell size RRM 1 (Os-csRRM1) and Oryza sativa cell size RRM 2 (Os-csRRM2), respectively. Both of them exhibit a high degree of evolutionary conservation in plant. For Os-csRRM2, significant homology was observed in Triticum aestivum (90% identity), Hordeum vulgare (90% identity), Lolium perenne (82% identity), Zea mays (81% identity),Ricinus communis (76% identity), Vitis vinifera (68% identity), Arabidopsis thaliana (68% identity) and Brassica napus (64% identity) (Fig. 1). The high degree of conservation suggests that this RRM domain might have similar function in different plants. Indeed, we observed that overexpression of Bn-csRRM2 also increased the cell size of B. napus (unpublished data). As cotton fiber length is a key factor in cotton yield and quality, we investigated whether this attribute could be enhanced by constitutive expression of Bn-csRRM2. Transgenic and wild-type cotton were grown in same condition. The leaves of 25 day and 45 day plants were harvested for microarray analysis. RNA samples were isolated from 3 biological replications using TRIzol (Invitrogen) as described by the manufacturer. Microarray analyses were carried out using Agilent Cotton Gene Expression Microarray (G2519F-022523). Microarrays were scanned on Agilent Technologies Scanner G2505C and data points were extracted using Agilent Feature Extraction software (Version 10.7.1.1). Comparisons were made between transgenic samples and their corresponding wild-type samples.
2011-12-31 | E-GEOD-26445 | biostudies-arrayexpress
Project description:With the onset of resistance, ovarian cancer cells display almost unpredictable adaptive potential. This may derive from genetic ancestry of the tumor cells and can be additionally tailored by post translational protein modifications (PTMs). The latter are profoundly shaped by the physical and chemical cues of the cancer microenvironment which, for ovarian cancer, is primarily the abdominal cavity. In this study, we took advantage of high-end proteome and phosphoproteome analyses combined with multiparametric morphometric profiling for the description of the proteome signatures of high-grade serous carcinomas (OVCAR-3) and non-serous carcinomas (SKOV-3) ovarian cancer cells. For the functional experiments, we applied two different protocols, representing typical stimuli of the peritoneal cavity and of the growing tumor mass: on the one side hypoxia (oxygen 1%) which develops within the tumor mass or is experienced during migration/extravasation in non-vascularized tissues. For comparison, fluid shear stress (2.8 dyn/cm2, orbital shaker method) which characterizes the tumor surface in peritoneal cavity or metastases spread in the bloodstream. After 3 hours incubation, treatment groups were clearly distinguishable by PCA analysis. Whereas basal proteome profile of SKOV-3 and OVCAR-3 cells appeared almost unchanged, phosphoproteome analysis revealed multiple regulations. These affected primarily cellular structure and proliferative potential and consolidated after 24h treatment. Albeit maintaining their individuality, hypoxia modified cell metabolism and morphology of both OVCAR-3 and SKOV-3: upon oxygen reduction cell size increased in concerted regulation of pathways related to Rho-GTPases and/or cytoskeletal elements (proteome and phosphoproteome). Also shear stress stimulation sharpened the response profile of SKOV-3 and OVCAR-3: this retraced their pathophysiological behavior and actively modified structural proteins as well as metabolism (e.g. delta(14)-sterol reductase, Kinesin-like proteins (KIF-22/20A) and Actin-related protein 2/3 complex). In conclusion, we characterized a biochemical and structural fingerprinting describing the adaptive potential of ovarian cancer cells to physical/chemical stressors typical for the abdominal cavity.
2022-01-13 | PXD027466 | Pride
Project description:Epithelial ovarian carcinoma (EOC) is an aggressive tumor often diagnosed at an advanced stage, when there is little prospect for cure. Despite some advances in surgical and chemotherapeutic strategies, only marginal improvements in patient outcome have been obtained. Hence, understanding the biological mechanisms underpinning EOC progression is critical for its treatment and to ameliorate patients survival. Recently, we reported that CD157 is expressed in EOC and controls tumor cell migration and invasion. Using stable overexpression and knockdown in OVCAR-3 and OV-90 ovarian cancer cell lines, we demonstrated that CD157 overexpression promotes morphological and functional changes, characterized by downregulation of epithelial marker and upregulation of mesenchymal ones. These are mediated at the transcriptional level by altering the expression of Snail and Zeb1 transcriptional repressors. The effects of CD157 overexpression on ovarian cancer phenotype translate into increased tumor cell motility and mesotelial invasion, while its knockdown significantly reduces the migratory potential, implying a direct correlation between CD157 expression levels and EOC aggressiveness. The analysis of the transcriptomic profiling highlighted 378 significantly differentially expressed genes, representing the signature of CD157-overexpressing EOC cells. The overall picture deduced from the analysis of these modulated transcripts indicated that high CD157 expression results in strengthening of a number of biological functions that favour tumor progression (including cell differentiation, cell motility and migration), and weakening of selected biological processes that hinder the tumor progression (such as apoptosis, cell death and response to stress). Collectively, these data support a causal role of CD157 in the control of ovarian cancer progression motivating the existence of a direct correlation between the expression levels of CD157 and the adverse clinical outcome in EOC patients, and suggest that CD157 may represent a valuable therapeutic target. Gene expression analysisi of control cell lines (OVCAR-3/mock and OV-90/mock) and testing cell lines (OVCAR-3/CD157 and OV-90/CD157), with two replicates, with dye swap, performed for each sample.
2012-12-31 | E-GEOD-36364 | biostudies-arrayexpress