50uM Casodex treatment of LNCaP Prostate Cancer cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Randy Jeffrey
PROVIDER: E-GEOD-8533 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Genome wide expression changes following 50uM Casodex treatment were investigated to determine regulatory targets commonly overlooked in gene function specific microarrays and for comparison of the effects the wild-type AR expressing PC-346C cells against the mutant androgen receptor (AR) LNCaP cell line. PC-346C Prostate Cancer cells were treated for a period of 48h with or without 50uM Casodex following a 36h seeding period. At the selected time point, total RNA was harvested from the cells for hybridization and analysis by Nimblgen Systems Inc using the homo sapiens gene expression array.
2007-09-15 | E-GEOD-8534 | biostudies-arrayexpress
Project description:Genome wide expression changes following treatment with the HDACs (Histone Deacetylase Inhibitor) CG-1521 (7.5uM) or TSA (Trichostatin A) were investigated to determine regulatory targets and patterns of the HDAC Inhibitors. LNCaP Prostate Cancer cells were treated for a period of 24h with either CG-1521 (7.5uM) or TSA (5uM) following a 24h seeding period. At the selected time point, total RNA was harvested from the cells for hybridization and analysis by Nimblgen Systems Inc using the homo sapiens gene expression array.
2007-09-15 | E-GEOD-8645 | biostudies-arrayexpress
Project description:We previously encountered regulatory processes where dihydrotestosterone (DHT) exerted its inhibitory effect on parathyroid hormone-related protein (PTHrP) gene repression through the estrogen receptor (ER)M-NM-1, but not the androgen receptor (AR) in breast cancer MCF-7 cells. Here, we investigated whether such an aberrant ligand-nuclear receptor (NR) interaction is present in prostate cancer LNCaP cells. First, we confirmed that LNCaP cells expressed a functional AR and at negligible levels of ERM-NM-1, and progesterone receptors. Both suppression of PTHrP and activation of the PSA genes were observed after treatment of E2, DHT and R5020. Consistent with the previous notion that the AR in LNCaP cells lost the ligand specificity due to a mutation AR (Thr-Ala877), our study using siRNA targeting each NR revealed that the AR, but not the other NRs, monopolized the role as the mediator of shared hormone-dependent regulation. These results were invariably associated with nuclear translocation of this mutant AR. Microarray of the genes regulated by either DHT, E2 or R5020 downstream of the AR (Thr-Ala877) revealed that more than half genes overlapped in LNCaP cells. Noticeably, AR (wild-type, wt) and AR (Thr-Ala877) were equally responsible for the E2-AR interactions. Fluorescent microscopic experiments demonstrated that both EGFP-AR (wt) and EGFP-AR (Thr-Ala877) were exclusively localized within the nucleus after E2 or DHT treatment. Further, a promoter assay revealed that breast cancer MCF-7 and Rv22 cells also exhibited such an aberrant E2-AR (wt) signaling. We postulate entangled interactions between the AR (wt) and E2 in a certain hormone-sensitive cancer cells. Total RNAs from the LNCaP cells transfected with control siRNA (siCT) or siRNA for AR (siAR) transfected LNCaP cells before 24 hr followed by exposed to 10-7M of DHT, E2 or R5020 exposure for another 24 h, respectively, were used.
2014-06-19 | E-GEOD-58615 | biostudies-arrayexpress
Project description:The androgen receptor (AR) mediates the action of androgens by binding to androgen-responsive elements (AREs) and subsequently regulating target genes involved in prostate carcinogenesis. The precise locations, true nature, and functional roles of AREs in human prostate cancer are still unknown. Here we redefine AREs by motif-resolution AR chromatin immunoprecipitation-exonuclease (ChIP-exo) assay in human prostate cancer cells and tumors. Surprisingly, we find that, in addition to canonical full-length AREs and half-site-like AREs, a significant portion of the four redefined ARE categories comprises non-canonical full-length AREs. The redefined AREs in enhanced AR binding regions in prostate tumors versus paired non-malignant adjacent tissues regulate a prostate cancer-relevant gene network not only centered on AR, but more interestingly, on novel AR target genes mTOR, BIRC5 and BCL2L1 involved in prostate cancer cell growth and survival. The precise redefinition of AREs has important implications for understanding how AR contributes to prostate carcinogenesis. To examine the differential AR binding in LNCaP cells before and after androgen stimulation, ChIP-Seq of androgen receptor is performed in LNCaP cells under the two conditions. To profile histone modification status in control LNCaP cells, MNase-Seq is performed with five different antibodies specific to certain histone marks. Each experiment includes two replicates.
2015-01-01 | E-GEOD-43720 | biostudies-arrayexpress
Project description:Prostate cancer is the most common cancer in men and cardiac glycosides inhibit prostate cancer cell proliferation. In order to investigate the mechanism by which cardiac glycosides inhibit prostate cancer cells, we observed genome-wide RNA expression in prostate cancer LNCaP-abl cells, hormone resistant cells, after the cardiac glycoside treatment using RNA-Seq. In addition, we profiled LNCaP-abl cells after androgen receptor (AR) knockdown to observe whether cardiac glycoside effect on RNA expression is similar to that of AR knockdown. Observation of three cardioglycosides, Digoxin, Peruvoside and Strophanthidin, and AR knockdown regulated RNA expression in LNCaP-abl with RNA-Seq (each triplicates)
2012-04-03 | E-GEOD-35126 | biostudies-arrayexpress
Project description:Detailed analysis of androgen regulated gene expression in the LNCaP prostate cancer cell line. Since androgens and the AR are known to be important for prostate cancer cell proliferation and invasion we aimed to identify androgen receptor (AR) regulated genes by combining this detailed Illumina beadarray study of androgen regulated gene expression with AR ChIP-sequencing data. LNCaP cells were grown in RPMI medium supplemented with 10% charcoal dextran stripped (steroid depleted) FBS for 72h, before treatment with 1nM R1881 or vehicle control. Total RNA was harvested every 30min for 4h and then every hour up to 24h using trizol (Sigma), quantified using a Nanodrop spectrophotometer (ND-1000). RNA samples were prepared for analysis on Illumina Human 6 v2 BeadArrays and Biotrove Realtime PCR panels according to the manufacturers protocols (see Supplementary Methods for details). Expression array data were normalised in R using the beadarray software and BASH (see Supplementary Methods for details) (Cairns et al., 2008; Dunning et al., 2007). 48 total RNA samples from LNCaP cells grown for 72h in RPMI supplemented with 10% charcoal dextran stripped FBS, comprising: 3 time zero samples; 10 vehicle (ethanol) control samples taken at 2h, 4h, 8h, 12h, 24h in duplicate; 36 androgen (R1881) treated samples taken every 30min for 4h then every hour until 24h following treatment (with replicates at 1h, 2h, 4h, 8h, 12h, 16h, 20h, 24h) The Illumina HumanWG v2 BeadArrays consist of two replicate sections that we treat as technical replicate arrays for the purposes of this analysis due to small but systematic shifts between sections that need to be addressed in the normalization. Data were analysed from the raw bead-level using the beadarray software, with spatial artefacts identified and removed automatically (BASH) and curated manually (Cairns et al., 2008; Dunning et al., 2007)
2010-09-01 | E-GEOD-18684 | biostudies-arrayexpress
Project description:Genome wide expression changes following 50uM Casodex treatment were investigated to determine regulatory targets commonly overlooked in gene function specific microarrays and for comparison of the effects the wild-type AR expressing PC-346C cells against the mutant androgen receptor (AR) LNCaP cell line. Keywords: Expression response to treatment, will be used with another array dataset for cell type comparison.
2007-09-15 | GSE8534 | GEO
Project description:Genome wide expression changes following 50uM Casodex treatment were investigated to determine regulatory targets commonly overlooked in gene function specific microarrays and for comparison of the effects of the mutant androgen receptor (AR) LNCaP cell line against the wild-type AR expressing PC-346C cells. Keywords: Expression response to treatment, will be used with another array dataset for cell type comparison.
2007-09-15 | GSE8533 | GEO
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare AR binding activity in LNCaP cells with and without knockdown of GATA2. Methods: LNCaP cells between passage number 32-34 were used for assay. Cells are transfected with GATA2 specific or nonspecific siRNA and ChIP was performed, the ChIP producted was further used to generate library with illumina ChIP-seq kit. Hi-seq 2500 was used for sequencing and the data was analyzed by MACs for peaks. Results: GATA2 knockdown lead to changes of AR binding activity , in most AR binding sites, AR shows decreased bindig activity. Only small percent sites show increased binding. Conclusions: Our study represents the first detailed analysis of the relationship between GATA2 and AR binding in whole genomic DNA.These results demostrate GATA2 play a critical role in AR activity in prostate cancer. LNCaP cells was used as cell model were treated with specific GATA2 siRNA.Library was sequenced using Illumina HI-seq 2500.
2014-01-21 | E-GEOD-52725 | biostudies-arrayexpress
Project description:A small molecule compound, here called 154, has a dual inhibitor effect of IL6/STAT3 and AR pathway, which reduces AR and STAT3 transcriptional activity in LNCaP cells. To profile the effected genes by compound 154 prostate LNCaP cells were treated with DMSO and compound 154 at 1 uM and 0.4 uM in duplicates in 6-well plate, cells were harvested at 24 hours. All the cells were harvested and total RNA was extracted using Qiazol method followed by Agilent DNA microarray analysis.
2018-07-01 | E-MTAB-5102 | biostudies-arrayexpress