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

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

PROVIDER: PRJNA837218 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19168516.fastq.gz	Fastqsanger.gz
	SRR19168517.fastq.gz	Fastqsanger.gz
	SRR19168518.fastq.gz	Fastqsanger.gz
	SRR19168519.fastq.gz	Fastqsanger.gz
	SRR19168520.fastq.gz	Fastqsanger.gz

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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

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

Genome-wide CRISPR Knockout Screen in LNCaP Cells Treated with Enzalutamide

Project description:To categorize gene loss events in enzalutamide-treated LNCaP cells, a genome-wide CRISPR knockout (KO) screen was performed. We quantified sgRNA abundance between initial and final timepoints in DMSO and enzalutamide treated cell populations

2024-09-30 | GSE226977 | GEO

Expression data from LNCaP cells treated with DHT and enzalutamide

2013-04-01 | GSE44905 | 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.

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The effects of enzalutamide on androgen-dependent and androgen-independent prostate cancer cells.

Project description:To investigate the mechanisms of drug resistance and castration resistance in prostate cancer, we performed proteomic sequencing on androgen-dependent prostate cancer cells (LNCaP) and androgen-independent cells (AI) treated with enzalutamide.

2024-11-26 | PXD058261 |

RNA-Sequencing Analysis of LNCaP Wildtype (WT) and RB-p53 CRISPR-Cas9 Double Knockout (DKO) Cells Treated with Enzalutamide

Project description:To investigate differential gene expression between LNCaP wild type (WT) cells and cells deficient for RB and p53 in the presence of absence of enzalutamide To investigate differential gene expression between LNCaP wild type (WT) cells and cells deficient for RB and p53 (generated using CRISPR-Cas9) in the presence of absence of enzalutamide

2024-09-30 | GSE226978 | GEO

Acquired Resistance to the Second-Generation Androgen Receptor Antagonist Enzalutamide in Castration-Resistant Prostate Cancer

Project description:Illumina gene array analyses of prostate cancer cell lines that had acquired resistance to Enzalutamide (MDV3100). mRNA analyses of four cell lines (CWR-R1, LAPC-4, LNCaP, and VCAP) cells that were either untreated, treated for 48hrs with Enz (short-term), or continuously grown in Enzalutamide for >6 months.

2016-02-24 | E-GEOD-78201 | biostudies-arrayexpress

RNA-sequencing of LNCaP prostate cancer cells with and without treatment of enzalutamide

Project description:LNCaP prostate cancer cells were stimulated with the synthetic androgen R1881. RNA-sequencing was performed to identify changes induced by enzalutamide treatment on the transcriptome level.

2023-02-15 | GSE220097 | GEO

MYC-mediated ribosomal gene expression sensitizes enzalutamide-resistant cells to EP300/CREBBP inhibitors

Project description:Various mechanisms have been reported to be responsible for enzalutamide resistance in prostate cancer. In our previous studies, we have demonstrated that the histone acetyltransferase EP300 is highly expressed in castration therapy-resistant prostate cancer. In the present study, we investigated the role of EP300/CREBBP in enzalutamide-resistant prostate cancer. Enzalutamide resistant and control DuCaP cells generatd previously were treated with histone acetyltransferase (C646) and bromodomain (I-CBP112) inhibitors of EP300/CREBBP. Additionally Enzalutamide resistant cells under 5 µM enzalutamide treatment and control LNCaP cells were analyzed. DuCaP and LNCaP cells were seeded in 6-well-plates at 8 x 10^5 and 6 x 10^5 cells per well. The following day, DuCaP cells were treated with 8 µM enzalutamide, 10 µM C646, 10 µM I-CBP112 or DMSO equivalent for 24 hr.

2021-02-17 | GSE163240 | GEO

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