Project description:Defective in Cullin Neddylation 1 Domain Containing 1 (DCUN1D1) is an E3 ligase for neddylation, a post translational process similar to, and that runs in parallel with the ubiquitin proteasome pathway. Although being established as an oncogene in various squamous cell carcinomas, the role of DCUN1D1 in prostate cancer has not been explored. Here we used microarray analysis to determine the set of genes regulated by DCUN1D1 in prostate cancer cells. Using the prostate cancer DU145 cell line as model, and a lentivirus encoding shRNA-DCUN1D1, we generated DCUN1D1 knockdown cell lines. Microarray analysis identified deregulation of key gene expression, cellular growth and proliferation, developmental, cell death and cancer pathways as possible mechanisms mediated by DCUN1D1 in prostate cancer.
Project description:Comparison of non-coding RNA profiling by array in sublines of DU145 human prostate cancer cell lines created by in vivo cycling Cell lines created by removal and growth of metastatic human DU145 tumor cells from mouse lymph node (metastasized from prostate xenograft) for LN cells and extracted from lung after intravenous injection (ivLU cells). Cell line numebr represented number of in vivo cycles of metastatic selection
Project description:To investigate the anti-tumor function of compound H93 in the development of prostate cancer, we treated DU145 cell lines with H93, SAHA or DMSO. We then performed gene expression profiling analysis using data obtained from RNA-seq of cells after treatment.
Project description:Activation of Signal Transducer and Activator of Transcription 3 (STAT3) is common in prostate cancers. STAT3 may induce cell proliferation and resistance to apoptosis, as well as promote tumor angiogenesis, invasion, and migration by activating gene expression. Many STAT3-dependent transcriptional responses are mediated through protein-protein interactions that involve the amino-terminal domain (N-domain). In this study, we found that inhibition of the STAT3 N-domain using novel inhibitor ST3-Hel2A-2 induces apoptotic death in prostate cancer cells. The cell death was accomponied by robust activation of pro-apoptotic gene. Using chromatin immunoprecipitation and tiling human promoter arrays (ChIP-chip), we have defined genome-wide targets of STAT3 in DU145 prostate cancer cells. We found that upregulated pro-apoptotic genes were bound by STAT3 in prostate cancer cells, and that STAT3 binding was decreased following inhibition of the STAT3 N-domain. STAT3 siRNA knockdow confirmed specificity of STAT3 binding and changes in gene expression. DU145 cells were treated with STAT3 siRNA or scrambled siRNA for 48hr. Total RNA has been extracted and prepared for hybridization on Affymetrix HG-U133A 2.0 arrays.