Comparisons of the global gene profile between CLDN4-overexpressing and CLDN4-silencing ovarian cancer cells.
ABSTRACT: A microarray analysis was performed to compare the global gene expression profile between CLDN4-overexpressing (Control) and CLDN4-silencing SKOV-3 ovarian cancer cells. CLDN4 gene was knocked down by CLDN4 siRNA lentivirus. Total RNA was extracted and microarray was perfomed to compare the gene profiling changes between CLDN4-overexpressing (Control) and CLDN4-silencing cells. The experiment was performed in triplicate.
Project description:A microarray analysis was performed to compare the global gene expression profile between C-CPE treated- and untreated- SKOV-3 ovarian cancer cells. SKOV-3 cells were treated with or without C-CPE for 72 hours, and total RNA was extracted and microarray was perfomed to compare the gene profiling changes between C-CPE treated- and untreated- cells. The experiment was performed in triplicate.
Project description:We intraperitoneally injected SKOV3 (derived from human ovarian adenocarcinoma) expressing soluble fragment of human EP2 receptor or hIgG Fc (SKOV/ip-FuEP2/Ex2 and (SKOV/ip-Fumock). After 4 week, resulted tumors were lysed and total RNAs were isolated. By using microarray, We analyzed gene expression and identified distinct classes of up-regulated genes in SKOV/ip-FuEP2/Ex2-derived tumor. Tumor tissues from SKOV/ip-Fumock or SKOV/ip-FuEP2/Ex2 were lysed and total RNAs were extracted. And then we analyzed expression status by Affymetrix microarrays.
Project description:We performed a microarray experiment to assess SAHA-induced changes in expression of genes of the homologous recombination DNA repair pathway SKOV-3 ovarian cancer cells were treated with 1µM SAHA or vehicle-control (0.01% DMSO) for 6 or 24 hours, harvested and processed for RNA isolation. Data for both time-points for SAHA and vehicle-control treated cells were obtained in duplicate. Total RNA was isolated using the Qiagen RNeasy Kit (Qiagen, Valencia, CA) according to manufacturer's instructions. cDNA synthesis and hybridization on oligonucleotide microarrays (U133 Plus 2.0 Array GeneChip, Affymetrix, Inc., Santa Clara, CA) were carried out using standard protocols.
Project description:Xenograft ovarian tumors are useful model to test therapeutic candidates in vivo. We used microarrays to gain insight into the expression changes during tumor growth and induced by the vitamin D analog, MT19C at multiple time points. SKOV-3 cells were grown in 10% FBS/DMEM before injection into mice. Total RNA was collected using standard methods.
Project description:We are studying signaling pathways and growth properties of cultured human ovarian cancer cells that are expressing the G protein-coupled receptor, luteinizing hormone receptor (LHR),particularly interested in the changes that occur when the receptor is activated by its cognate ligand, gonadotropin (LH). To investigate these questions, we have employed the SKOV3 ovarian cancer cell line that has been stably transfected with LHR, and can then test the response of these cells in culture following exposure to LH. The parent SKOV-3 ovarian cancer cell line was chosen as a control in this study since it does not express LHR, and, following transfection, the LHR+ cells serve to determine the alterations in gene expression elicited by LH. The LHR+ cells bound human chorionic gonadotropin with a Kd of 0.3 nM (human chorionic gonadotropin and LH utilize the same G protein-coupled receptor, LHR), consistent with the binding affinity using ovarian reproductive cells, and responded to LH with increased intracellular levels of cAMP and inositol phosphates. In total, six groups of SKOV-3 cells (LHR-, LHR+, and LHR+ incubated with LH for various times: 1, 4, 8, and 20 h), each with three independent replicates, were used for examining the cell response.
Project description:We studied the variations of mRNA amounts after Evi1 knockdown or Flag-Evi1 overexpression in SKOV-3 cells. Despites Evi1 discovery in 1988, its recognized role as a dominant oncogene in myeloid leukemia and more recently in epithelial cancers, only a few target genes were known and it was not clear why Evi1 was involved in cancer progression. Here we obtained the genomic binding occupancy and expression data for Evi1 in human ovarian carcinoma cells. We identified numerous Evi1 target cancer genes and genes controlling cell migration and adhesion. Moreover, we characterized a transcriptional cooperation between AP1 and Evi1 that regulated proliferation and adhesion through a feed-forward loop. Furthermore, this study provides human genome-wide mapping and downstream analyses for Evi1 that will be useful for the research community. 16 samples were collected. Each condition was done in 4 replicates, collected 65 hours after transfection. Transfections with control siRNA or Flag-expressing vector were used as controls.
Project description:To identify the downstream targets of transcription factor Ascl1, transcriptional profiling of rat glial cell line, CG4 cell, transfected with either Ascl1 or mock control was performed. Comparison was performed between Ascl1 overexpressing CG4 cell and mock control transduced cell on 3D-Gene rat mRNA oligo 12k chip. Biological replication was not prepared. The results were confirmed by real time RT-PCR in several genes.
Project description:Identification of target genes of PITX2 homeodomain transcription factor in ovary using human ovarian adenocarcinoma cells, SKOV-3 to determine the transcriptional network of PITX2. Genotypic Technology designed Custom Human Promoter 244k ChIP-on-chip Array (AMADID-019469)
Project description:Kallikrein-related peptidase 7 (KLK7) is a serine peptidase that is over-produced in the most lethal form of ovarian cancer, called high grade serous ovarian cancer (HGSOC). To determine its underlying molecular mechanism of action, a comprehensive analysis of KLK7 degradome in the SKOV-3 cell-secreted proteins was performed using two complementary proteomic approaches, quantitative PROtein Topography and Migration Analysis Platform (qPROTOMAP) and Terminal Amine Isotopic Labelling of Substrates (TAILS).