Project description:celastrol is a natural product that affects LNCaP androgen-signalling by 24h; We used microarrays to detail the androgen-responsive program of gene expression affected by celastrol treatment at 24h Experiment Overall Design: LNCaP cells were grown to 50% confluency and deprived of androgen, and subsequently treated with celastrol plus androgen, androgen alone, or vehicle alone for 24h prior to direct Trizol lysis and RNA isolation
Project description:celastrol is a natural product that affects LNCaP androgen-signalling by 24h We used microarrays to detail the androgen-responsive program of gene expression affected by celastrol treatment at 24h Keywords: drug treatment
Project description:Gedunin is a natural product that affects LNCaP androgen-signalling by 24h; We used microarrays to detail the androgen-responsive program of gene expression affected by gedunin treatment at 24h Experiment Overall Design: LNCaP cells were grown to 50% confluency and deprived of androgen, and subsequently treated with gedunin plus androgen, androgen alone, or vehicle alone for 24h prior to direct Trizol lysis and RNA isolation
Project description:Global definition of androgen and anti-androgen effects on LNCaP transcriptomes using Affymetrix U133A oligonucleotide microarray. LNCaP in androgen-depleted medium was treated with androgen (DHT) and anti-androgen (CPA) for different time points (2 hours, 4 hours, 8 hours, and 24 hours). Untreated or Vehicle (Ethanol) treated samples as control.
Project description:Celastrol is a natural product that affects LNCaP gene expression by 6h; We used microarrays to detail the global programme of gene expression affected by celastrol treatment at 6h Experiment Overall Design: LNCaP cells were grown to 50% confluency and treated with celastrol for 6h prior to direct Trizol lysis and RNA isolation
Project description:Transcriptional profiling of the LNCaP cell line treated with R1881 synthetic androgen and/or cycloheximide. LNCaP cells were stimulated with R1881 alone, with cycloheximide alone, or with R1881 in the presence of cycloheximide for 24h and compared to control untreated cells. Two independent cell culture experiments for each treatment condition were performed for microarray analysis. Each experiment was repeated with a switch in fluorescent Cy3/Cy5 labels to account for dye effects to produce four data points per hybridization spot.
Project description:G-1 is an agonist to GPR30. Activation of GPR30 by G-1 inhibited prostate cancer cell growth in LNCaP xenografts regrown after catration of the host (nude mice), but not in the androgen-sensitive LNCaP xenograft grown in an intact host. Results provide insights into the molecular basis of G-1 action in castration-resistant prostate cancer. Male nude mice were injected with LNCaP cells. When the LNCaP tumors reached 150–300 mm3, mice were divided into two groups: intact (androgen-sensitive tumor) and castrated. For the intact group, mice were subcutaneously injected with vehicle alone (95% PBS, 2.5% DMSO, 2.5% ethanol) or G-1 (4 mg/kg/day in vehicle) daily for 16 days. For the castrated group, tumors regressed and then regrew to ~300-400mm3. Mice were treated daily with vehicle or G-1 as described for 16 days. Tumors were harvested for RNA extraction and microarray experiments.
Project description:Serum starved MDAMB453 cells were serum starved and treated for 4 hours with vehicle control (ethanol), 5α-dihydrotestosterone (DHT; 10nM) or medroxyprogesterone acetate (MPA; 10nM). AR binidng peaks were determined. Subsequent analysis showed that binding sites for androgen receptor are enriched at breast cancer risk loci.
