Expression data from LNCaP and abl cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE11428 | GEO | 2009/07/25
SECONDARY ACCESSION(S): PRJNA106451
REPOSITORIES: GEO
Similar Datasets
Project description:Androgen receptor (AR) is a ligand-dependent transcription factor that plays a key role in the onset and progression of prostate cancer. We investigated AR-induced gene expression in prostate cancer cells LNCaP and abl by transfecting siAR / siControl or treating cells with androgen (DHT) over a time course. Experiment Overall Design: We hybridized RNA to Affymetrix human genome U133 plus 2.0 arrays.
2009-08-07 | E-GEOD-11428 | 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: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.
2012-04-04 | GSE35126 | GEO
Project description:We introduce a family of multivalent peptidomimetic conjugates that modulate the activity of the androgen receptor (AR). Bioactive ethisterone ligands were conjugated to a set of sequence-specific peptoid oligomers. Certain multivalent peptoid conjugates enhance AR-mediated transcriptional activation. We identify a linear and a cyclic conjugate that exhibit potent anti-proliferative activity in LNCaP-abl cells, a model of therapy-resistant prostate cancer. The linear conjugate blocks AR action by competing for ligand binding. In contrast, the cyclic conjugate is active despite its inability to compete against endogenous ligand for binding to AR in vitro, suggesting a non-competitive mode of action. These results establish a versatile platform to design competitive and non-competitive AR modulators with potential therapeutic significance. We use microarray analysis to further elucidate the mechanism of AR antagonism and show that the compounds (cyc and n=8) are distinct. We used microarray analysis to see genone-wide effects on LNCaP-abl cells with moduators of AR activity LNCaP-abl cells were treated with compound and RNA was extracted and hybridized on Affymetrix microarrays Treatments: Vehicle is just Ethanol treated LNCaP-abl cells that were used as a control. n=8 and cyc are peptoid conjugates that modulate AR activity. n=8 is linear and cyc is a cyclic compounds. We wanted to look at gene expression when LNCaP-abl cells were treated with these compounds to show that they are distinct. C3 is a small molecule that inhibits the interaction between AR and beta-catenin (co-regulator protein). Initial results with this compound show potent anti-proliferative activity in LNCaP-abl cells and we wanted to further investigate the mechanism of action of this compound.
2012-12-21 | E-GEOD-37796 | biostudies-arrayexpress
Project description:We introduce a family of multivalent peptidomimetic conjugates that modulate the activity of the androgen receptor (AR). Bioactive ethisterone ligands were conjugated to a set of sequence-specific peptoid oligomers. Certain multivalent peptoid conjugates enhance AR-mediated transcriptional activation. We identify a linear and a cyclic conjugate that exhibit potent anti-proliferative activity in LNCaP-abl cells, a model of therapy-resistant prostate cancer. The linear conjugate blocks AR action by competing for ligand binding. In contrast, the cyclic conjugate is active despite its inability to compete against endogenous ligand for binding to AR in vitro, suggesting a non-competitive mode of action. These results establish a versatile platform to design competitive and non-competitive AR modulators with potential therapeutic significance. We use microarray analysis to further elucidate the mechanism of AR antagonism and show that the compounds (cyc and n=8) are distinct.
2012-12-21 | GSE37796 | GEO
Project description:Prostate cancer is dependent on androgen receptor (AR) signaling at all stages of the disease and cyclin D1 has been shown to negatively modulate the expression of the AR-dependent gene prostate specific antigen (KLK3/PSA). Unbiased gene expression profiling was performed to determine the androgen-regulated geneset that is sensitive to cyclin D1. Androgen-sensitive LNCaP cells were straved of androgen, then transduced with control green fluorescent protein (GFP) or cyclin D1 (CCND1) adenovirus, then subsequently stimulated with control (Ethanol) or dihydrotestosterone (DHT).
2011-01-07 | E-GEOD-26483 | biostudies-arrayexpress
Project description:5α-androstane-3α,17β-diol (3α-diol) is reduced from the potent androgen, 5α-dihydrotestosterone (5α-DHT), by reductive 3α-hydroxysteroid dehydrogenases (3α-HSDs). 3α-diol is believed to be a weak androgen, and has to be oxidized to 5α-DHT before it can exert its androgenic activity on androgen target tissues including the prostate. However, we repeatedly demonstrated that 3α-diol can be a potent androgen, activates cytoplasmic signaling pathway, and may be responsible for androgen-independent prostate cancer growth. A cancer-specific, cDNA-based membrane array was used to determine 3α-diol-mediated gene expressions in prostate cancer progression. Several canonical pathways appeared to be affected by 3α-diol-regulated signaling in LNCaP cells; among them are apoptosis signaling, PI3K/Akt signaling, and death receptor signaling pathways. Biological analysis of 3α-diol-activated signaling confirmed that 3α-diol augmented PI3K/Akt activation can be independent from the classical androgen receptor (AR) signaling. These observations sustained our previous report that 3α-diol continues to supported prostate cell survival and proliferation regardless the status of the AR. We provided the first global analysis of 3α-diol-activated gene expressions and identified cytoplasmic signaling pathways as important components of this response in human prostate cells. 3α-diol may play, therefore, a significant role for transition from androgen-dependent to androgen-independent prostate cancer progression in the presence of androgen blockade. Keywords: array, time course, androgen, prostate, cancer
2008-08-01 | GSE8860 | GEO
Project description:Androgen Receptor (AR) is essential for the growth and progression of prostate cancer in both hormone-sensitive and hormone-refractory disease. We have designed a sequence-specific DNA binding polyamide (1) that targets the consensus androgen response element (ARE). This polyamide binds the PSA promoter ARE, inhibits androgen-induced expression of PSA and several other AR-regulated genes in cultured prostate cancer cells, and reduces AR occupancy at the PSA promoter and enhancer. Down-regulation of PSA by this polyamide was comparable to that produced by the synthetic anti-androgen bicalutamide (Casodex) at the same concentration. Genome-wide expression analysis reveals that a similar number of transcripts are affected by treatment with the polyamide and with bicalutamide. Direct inhibition of AR-DNA binding by sequence-specific DNA binding small molecules could offer an alternative approach to antagonizing AR activity. A polyamide (2) that targets a different DNA sequence is included as a control. Experiment Overall Design: DHT (dihydrotestosterone)-stimulated LNCaP cells that were treatment with polyamide 1, polyamide 2, bicalutamide were compared to control cells that were also DHT-stimulated. Cells not stimulated with DHT were also compared to the DHT-stimulated controls. Three biological replicates were included for each treatment/condition except the no-DHT induced controls, which were in biological duplicate.
2009-04-23 | E-GEOD-7708 | biostudies-arrayexpress
Project description:Enzalutamide (formerly MDV3100 and available commercially as Xtandi), a novel androgen receptor (AR) signaling inhibitor, blocks the growth of castration-resistant prostate cancer (CRPC) in cellular model systems and was shown in a clinical study to increase survival in patients with metastatic CRPC. Enzalutamide inhibits multiple steps of AR signaling: (1) binding of androgens to AR, (2) AR nuclear translocation, and (3) association of AR with DNA. Here we used Affymetrix human genome microarray technology to investigate the global programme of gene expression of LNCaP cells in response to enzalutamide alone and in the context of DHT-stimulated androgen receptor gene expression. LNCaP cells were grown in RPMI 1640 supplemented with 5% hormone depleted FBS and treated with vehicle (control sample) , DHT (100 nM), enzalutamide (1 or 10 M-BM-5M) or DHT (100 nM) plus enzalutamide (1 or 10 M-BM-5M)for 16 hours for RNA extraction and hybridization. Each condition was done in triplicate.
2013-04-01 | E-GEOD-44905 | biostudies-arrayexpress
Project description:Androgen receptor (AR) signalling pathway plays an important role in carcinogenesis and development of prostate cancer. The involvement of microRNA (miRNA) in this process is still largely unknown. In this study, we performed a matched miRNA-mRNA time-course expression profiling to reveal androgen response in hormone-sensitive prostate cancer cells.We introduced novel statistics Response Score (RS) and Modulation Score (MS) to identify significant androgen-regulated target genes and miRNA-modulated target mRNAs. Based on the analysis, we found several novel androgen-regulated targets, which had significant androgen response in expression pattern, and were highly enriched in predicted androgen responsive elements (AREs). AR-bindings to these AREs were validated with ChIP assay. Furthermore, a set of target mRNAs involved in crucial processes of tumor progression were identified to be significantly regulated by these miRNAs. Therefore, a miRNA-mediated androgen signalling network was inferred, including three novel feedback mechanisms for AR self-modulation. In conclusion, our study provides new approaches to further miRNA regulation research and contributes novel findings into miRNA-mediated pathological effects in prostate cancer. Total RNA obtained from androgen dihydrotestosterone (DHT) subjected to LNCaP cells in vitro at 20min, 40min, 1h, 2h, 4h, 8h, 16h, 24h and 48h, compared to the control at 0h.
2011-12-31 | E-GEOD-21245 | biostudies-arrayexpress