Project description:Transcription factor Stat5 is constitutively active in human prostate cancer but not in normal prostate epithelium. Stat5 activation is associated with prostate cancer lesions of high histological grades, and is present in the majority of castration-resistant recurrent human prostate cancers. The molecular mechnisms underlying constitutive activation of Stat5 in primary and recurrent human prostate cancer are currently unclear. We used microarrays to detail gene expression regulated by Stat5 in human prostate cancer cells. DU145 human prostate cancer cells were transfected with Stat5a/b siRNA or scramble siRNA as control. After 48 h, the cells were harvested and total RNA was prepared for Affymetrix microarrays.
Project description:Identification of the molecular changes that promote viability and metastatic behaviour of prostate cancer cells is critical for the development of improved therapeutic interventions for prostate cancer. Stat5a/b and Stat3 are both constitutively active in locally-confined and advanced prostate cancer, and both transcription factors have been reported to be critical for the viability and growth of prostate cancer cells. We used microarrays to compare gene expression profiles regulated by Stat5a/b vs. Stat3 in human prostate cancer cells. DU145 and CWR22Rv1 human prostate cancer cells were transfected with Stat3 siRNA, Stat5a/b siRNA or scramble siRNA as control. After 48 h, the cells were harvested and total RNA was prepared for Affymetrix microarrays.
Project description:Analysis of AR-regulation of gene expression. The hypothesis tested in the present study was that AR influences the expression of genes that participate in important bioprocesses in prostate cancer cells, including cell cycle, DNA replication, recombination and repair. Results provide important information on AR-responsive genes that may be crucial to the cell survival and the progression of prostate cancer. Total RNA obtained from AR siRNA-transfected prostate cancer cells compared to negative control siRNA-transfected prostate cancer cells 48 h after siRNa transfection.
Project description:Analysis of c-Myb-regulation of gene expression. The hypothesis tested in the present study was that c-Myb influences the expression of specific sets of genes that are involved in cell cycle, DNA replication, recombination and repair. Results provide important information on c-Myb-responsive genes that may be crucial to the cell survival and the progression of prostate cancer. Total RNA obtained from c-Myb siRNA-transfected prostate cancer cells compared to negative control siRNA-transfected prostate cancer cells 48 h after siRNa transfection.
Project description:C4-2B prostate cancer cells were transfected with siRNA against a non-specific (NS) sequence, siRNA specifically targeting EP300, or siRNA specifically targeting CREBBP. We tested the hypothesis that their exists different subgroups of genes that are preferentially affected by p300 or CBP depletion.
Project description:The human HOTAIR-specific siRNA and control siRNA were transfected into MCF-7-TNR cells. RNA was collected at 72 hrs after transfection. RNA-SEQ was carried out to profile the gene expression altered by HOTAIR knockdown.
Project description:SPOP is a ubiquitin ligase adaptor frequently mutated in prostate cancer. It is involved in ubiquitination and degradation of substrate proteins. We examined the impact of wild-type and mutant SPOP on the transcriptional profile of prostate cancer cells. We cloned several naturally occurring (in human prostate cancer) SPOP mutants and expressed the corresponding constructs in prostate cancer cells. Our experimental conditions were: Human prostate cancer cells (LNCaP-Abl), transfected with control vector, SPOP-wt, and any of the following mutants: SPOP-F102C, SPOP-F133V, SPOP-F133L (2-4 biological replicates each). We analyzed their gene expression profiles for differences induced by SPOP-wt vs SPOP-mutant.
Project description:The transcription factor HOXC6 is upregulated in human prostate cancer. SiRNA knockdown of HOXC6 induces apoptosis in LNCaP cells while upregulation rescued LNCaP cells from siRNA-induced apoptosis. We used microarrays to identify the genes whose expression underly the anti-apoptotic and proliferative effects of HOXC6 in LNCaP cells. Experiment Overall Design: LNCaP cells were transiently transfected with a cocktail of 5 siRNAs to HOXC6 to a final concentration of 100nM, with a HOXC6 gene expression vector, or control siRNA and vector. Cells were collected a 48hours post-transfection