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Effect of castration, bicalutamide, and enzalutamide on androgen receptor binding in Hi-Myc mouse prostate tumors

ABSTRACT: Effect of castration, bicalutamide, and enzalutamide on androgen receptor binding in Hi-Myc mouse prostate tumors

ORGANISM(S): Mus musculus

PROVIDER: GSE62645 | GEO | 2015/10/01

SECONDARY ACCESSION(S): PRJNA264711

REPOSITORIES: GEO

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Transriptome analysis of LNCaP/AR cell line after concomittant treatment with androgen with bicalutamide and enzalutamide

Project description:Transriptome analysis of LNCaP/AR cell line after concomittant treatment with androgen with bicalutamide and enzalutamide

2015-10-01 | GSE62474 | GEO

Transriptome analysis of VCAP and CWR22-Pc cell lines after concomittant treatment with androgen with bicalutamide and enzalutamide

Project description:Transriptome analysis of VCAP and CWR22-Pc cell lines after concomittant treatment with androgen with bicalutamide and enzalutamide

2015-10-01 | GSE62473 | GEO

Transriptome analysis of Hi-Myc prostate tumors after castration and antiandrogen treatment

Project description:Transriptome analysis of prostate tumors from Hi-Myc mouse prostates 3 days after castration or treatment with bicalutamide or enzalutamide

2015-10-01 | GSE62644 | GEO

Cellular androgen content influences enzalutamide agonism of F877L mutant androgen receptor

Project description:Prostate cancer is the most commonly diagnosed and second-most lethal cancer among men in the United States. The vast majority of prostate cancer deaths are due to castration-resistant prostate cancer (CRPC) â?? the lethal form of the disease that has progressed despite therapies that interfere with activation of androgen receptor (AR) signaling. One emergent resistance mechanism to medical castration is synthesis of intratumoral androgens that activate the AR. This insight led to the development of the AR antagonist enzalutamide. However, resistance to enzalutamide invariably develops, and disease progression is nearly universal. One mechanism of resistance to enzalutamide is an F877L mutation in the AR ligand-binding domain that can convert enzalutamide to an agonist of AR activity. However, mechanisms that contribute to the agonist switch had not been fully clarified, and there were no therapies to block AR F877L. Using cell line models of castration-resistant prostate cancer (CRPC), we determined that cellular androgen content influences enzalutamide agonism of mutant F877L AR. Further, enzalutamide treatment of AR F877L-expressing cell lines recapitulated the effects of androgen activation of F877L AR or wild-type AR. Because the BET bromodomain inhibitor JQ-1 was previously shown to block androgen activation of wild-type AR, we tested JQ-1 in AR F877L-expressing CRPC models. We determined that JQ-1 suppressed androgen or enzalutamide activation of mutant F877L AR and suppressed growth of mutant F877L AR CRPC tumors in vivo, demonstrating a new strategy to treat tumors harboring this mutation. RNA-seq profiles of prostate cancer cell lines to understand gene expression associated with enzalutamide treatment

2016-06-10 | E-GEOD-69896 | biostudies-arrayexpress

RNA sequencing of LNCaP cells treated with castration and/or enzalutamide

Project description:The goal of this study was to determine how androgen receptor inhibition alters transcriptional programs in prostate cancer cells. LNCaP prostate cancer cells were grown in 10% charcoal-stripped serum (CSS) supplemented with 0.5 nanomolar dihydrotestosterone (DHT), in CSS without DHT modeling castration, with CSS + DHT but in the presence of 10 micromolar enzalutamide, or in CSS without DHT (castrated) and in the presence of enzalutamide for 72 hours. Analysis shows that androgen receptor target genes are reduced with castration, enzalutamide or the combination of castration + enzalutamide.

2022-05-12 | GSE202755 | GEO

Cellular androgen content influences enzalutamide agonism of F877L mutant androgen receptor

Project description:Prostate cancer is the most commonly diagnosed and second-most lethal cancer among men in the United States. The vast majority of prostate cancer deaths are due to castration-resistant prostate cancer (CRPC) – the lethal form of the disease that has progressed despite therapies that interfere with activation of androgen receptor (AR) signaling. One emergent resistance mechanism to medical castration is synthesis of intratumoral androgens that activate the AR. This insight led to the development of the AR antagonist enzalutamide. However, resistance to enzalutamide invariably develops, and disease progression is nearly universal. One mechanism of resistance to enzalutamide is an F877L mutation in the AR ligand-binding domain that can convert enzalutamide to an agonist of AR activity. However, mechanisms that contribute to the agonist switch had not been fully clarified, and there were no therapies to block AR F877L. Using cell line models of castration-resistant prostate cancer (CRPC), we determined that cellular androgen content influences enzalutamide agonism of mutant F877L AR. Further, enzalutamide treatment of AR F877L-expressing cell lines recapitulated the effects of androgen activation of F877L AR or wild-type AR. Because the BET bromodomain inhibitor JQ-1 was previously shown to block androgen activation of wild-type AR, we tested JQ-1 in AR F877L-expressing CRPC models. We determined that JQ-1 suppressed androgen or enzalutamide activation of mutant F877L AR and suppressed growth of mutant F877L AR CRPC tumors in vivo, demonstrating a new strategy to treat tumors harboring this mutation.

2016-06-10 | GSE69896 | GEO

Linking prostate cancer cell AR heterogeneity to distinct castration and Enzalutamide responses

Project description:Molecular mechanisms underlying resistance to androgen deprivation therapy (ADT) and, in particular, to antiandrogen Enzalutamide, in treating castration-resistant prostate cancer (CRPC), remain incompletely understood. Through screening >120 CRPC patient samples, we observed 3 expression patterns of androgen receptor (AR) protein: primarily nuclear (nuc-AR), mixed nuclear/cytoplasmic expression (nuc/cyto-AR), and low/no expression (AR-/lo). Xenograft CRPC modeling in 4 models (i.e., LNCaP, VCaP, LAPC4, and LAPC9) recapitulated the 3 AR expression patterns in castration-resistant tumors developed from parental androgen-dependent tumors. Strikingly, although the 3 CRPC models that retained AR expression (LNCaP, VCaP, and LAPC4) responded, to different levels and in different kinetics, to Enzalutamide, the AR-/lo LAPC9 CRPC was completely refractory to Enzalutamide. By combining whole-genome RNA-Seq and biochemical analyses together with experimental combinatorial therapy in the LNCaP and LAPC9 models, we identified BCL-2 as a critical therapeutic target in both AR+/hi and AR-/lo, Enzalutamide-resistant CRPC models.

2018-08-01 | GSE88752 | GEO

LNCAP in-vitro treatment with androgen receptor targeting drugs

Project description:Gene expression in LNCaP cells after treatment with the androgen receptor targeting drugs bicalutamide (BIC), enzalutamide (ENZ) and apalutamide (ARN) in the presence or absence of dihydrotestosterone (DHT).

2022-09-07 | GSE211781 | GEO

Expression data from LNCaP cells treated with DHT and enzalutamide

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

RNA sequencing of 16D CRPC cells treated with enzalutamide over varying periods of time

Project description:The goal of this study was to determine how androgen receptor inhibition alters transcriptional programs in castration-resistant prostate cancer cells. 16D castration-resistant prostate cancer cells were grown in the presence of 10 micromolar enzalutamide for 24, 48, 96, 144 hours or for more than 2 months (long-term). Analysis shows that androgen receptor target genes are reduced with enzalutamide while metabolic genes are also differentially expressed.

2022-05-12 | GSE202885 | GEO

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