Project description:To discover the core gene expression features of CtBP1, CtBP2 differently regulated in ovarian cancer SKOV3 cells. The compared the whole transcript expression profiling between CtBP1 knockdown, CtBP2 knockdown and scramble control in ovarian cancer skov3 cells.
Project description:SRSF3 is overexpressed in human invasive ovarian cancer and its overexpression is required for cancer cell growth and survival. To decipher the mechnisms behind the role of SRSF3 in ovarian cancer, we examined the gene expression and splicing in the ovarian cancer cell line that was engineered to express a doxycycline-induced SRSF3 siRNA, which was able to knockdown SRSF3 expression by 90% and induce apoptosis. Total RNAs extracted from A2780/SRSF3si2, a subline of ovarian cancer cell line A2780, treated with or without doxycycline at 0.1ug/ml for three days were analyzed using Affymetrix GeneChip® Human Exon 1.0 ST Array
Project description:The anti-hypoxia capacity of ovarian cancer cells leads survive in stress tumor microenvironment intraperitoneal cavity. The identification of putative stress-induced factors may be used as target genes to impair the peritoneal metastases in ovarian cancer. In this study, a pool of ovarian cancer cells was treated by hypoxia (0.5% O2, 5% CO2, 24 h) or normoxia. Using transcriptional profiling (GeneChipTM Affymetrix Human Genome U133 Plus 2.0 Array) analysis, we identified BCL2A1 was a putative target gene protecting ovarian cancer cells against numerous stresses.
Project description:Stable Pax6 and Luciferase knockdown human embryonic stem cell lines (H9) were made through lentiviral infection. Two different Pax6 RNAi lines and two Luciferase RNAi lines were then differentiated to neuroectoderm cells for 6 days. mRNA pooled from these two individual lines were then subjected to gene expression profiling analysis using affymetrix U133 plus 2.0 array.
Project description:Deregulation of canonical Wnt/beta-catenin pathway is one of the earliest events in the pathogenesis of colon cancer. Mutations in APC or CTNNB1 (beta-catenin gene) are highly frequent in colon cancer and cause aberrant stabilization of b-catenin, which activates the transcription of Wnt target genes by binding to chromatin via the TCF/LEF transcription factors. Here we report an integrative analysis of genome-wide chromatin occupancy of b-catenin by chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq) and gene expression profiling by microarray analysis upon RNAi-mediated knockdown of beta-catenin in colon cancer cells (GSE53656). Immunoprecipitated samples from human colon cancer SW480 cells with antibodies against beta-catenin and control IgG respectively were used for ChIP-seq experiments.
Project description:The circadian clock is intricately connected with metabolism, however the precise details of these connections are incomplete. Here we used high temporal resolution metabolite profiling to determine circadian regulation of mouse liver and cell autonomous metabolism. In mouse liver, we found ~50% of metabolites were circadian, with strong enrichment of the nucleotide, amino acid, and methylation pathways. In U2OS cells, 27% of metabolites were circadian, including amino acids and NAD biosynthesis, also clock controlled in liver. To assess whether cell autonomous metabolite rhythms were clock-dependent, we used RNAi to perturb Bmal1, Cry1, and Cry2. Bmal1 knockdown eliminated most metabolite rhythms, while Cry1 generally shortened and Cry2 lengthened rhythms. Surprisingly, we found Cry1 knockdown induced 8 hr rhythms in amino acid, methylation, and vitamin metabolites, decoupling metabolite and transcriptional rhythms. These results provide the first comprehensive views of circadian liver and cell autonomous metabolism.
Project description:Genetically modified ovarian cancer cells were used to study the role of GBP1. Proteomics-based thermal stability assay (CETSA) was performed on GBP1 knockdown and overexpressing ID8 ovarian cancer cells. Shotgun proteomics was also performed on these cells.
Project description:Transcriptional profiling of untreated ovarian cancer cells and ovarian cancer cells miR-506 transfected with 48hours. Two-condition experiment, control vs. miR-506 treated cells. One replicate per array.
Project description:CCCTC-binding factor (CTCF) is an 11 zinc fingers transcription factor that functions as both an oncogenic and tumor suppressor, depending on the cancer types, through epigenetic regulation. Epigenetic regulation including DNA methylation and histone modifications are critically involved in cancer metastasis. We then hypothesized that CTCF might play a vital role in epithelial ovarian cancer metastasis. Firstly, we found that CTCF expression was elevated in ovarian cancer tissues compared to non-tumor tissues. The elevated expression of CTCF predicts poor prognosis of ovarian cancer patients. Then, we revealed that CTCF knockdown significantly inhibited the migration, invasion and metastasis of ovarian cancer cells, although it had no effect on cell proliferation and tumor growth, which have been demonstrated with both in vitro and in vivo experiments. More importantly, we observed a higher CTCF expression in metastatic lesions than that in primary lesions from ovarian cancer patients. Mechanically, PCR array demonstrated that CTCF might regulate a series of metastasis associated genes, including CTBP1, SERPINE1 and SRC. Finally, we observed positive correlations between CTCF expression and those three genes in epithelial ovarian cancer specimens. In conclusion, this study demonstrates that CTCF is an oncogene in ovarian cancer to promote tumor metastasis through broadly controlling the expression of metastasis-associated genes. Our findings suggest CTCF could be a novel drug target to treat ovarian cancer by interfering with cancer cell metastasis.