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Total RNA-Seq in TRAF4-overexpressing castration-resistant xenograft tumors and the control castration-responsive tumors

ABSTRACT: Total RNA-Seq in TRAF4-overexpressing castration-resistant xenograft tumors and the control castration-responsive tumors

PROVIDER: PRJNA644899 | ENA |

REPOSITORIES: ENA

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Total RNA-Seq in TRAF4-overexpressing castration-resistant xenograft tumors and the control castration-responsive tumors

Project description:We reported the tumor total gene expression TRAF4-overexpressing castration-resistant xenograft tumors and the control castration-responsive tumors

2020-07-15 | GSE154029 | GEO

Expression data from uncastrasion and castration tumor from LNCAP Orhotopic xenograft models of prostate cancer

Project description:To identify molecular singnal alterations between androgen dependent prostate cancer and castration resistant prostate cancer, we performed interspecies comparative microarray analyses using RNAs prepared from uncastrasion and castration tumor from LNCAP Orhotopic xenograft models of prostate cancer. microarray data from uncastrasion and castration tumor revealed that the gene expression profile is most significantly altered in between androgen dependent prostate cancer and castration resistant prostate cancer. Comparative analyses of LNCAP Orhotopic xenograft models of prostate cancer showed that genes involved in androgen dependent and androgen independent tumor were significantly altered. We prepared RNA samples from 4 samples uncastrasion and 4 samples castration tumors from LNCAP Orhotopic xenograft models of prostate cancer . High-quality RNA samples were subjected to microarray analysis using the Affymetrix Human Gene 2.0 ST platform, and only those results that passed examinations for quality assurance and quality control of the Human Gene 2.0 ST arrays were retrieved. In total, we obtained gene expression profiles from the following samples: 4 samples uncastrasion and 4 samples castration tumors

2013-04-20 | E-GEOD-46218 | biostudies-arrayexpress

Expression data from uncastrasion and castration tumor from LNCAP Orhotopic xenograft models of prostate cancer

2013-04-20 | GSE46218 | GEO

Identification of EP4 as a Potential Target for the Treatment of Castration-Resistant Prostate Cancer Using a Novel Xenograft Model

Project description:More effective therapeutic approaches for castration-resistant prostate cancer (CRPC) are urgently needed, thus reinforcing the need to understand how prostate tumors progress to castration resistance. We have established a novel mouse xenograft model of prostate cancer, KUCaP-2, which expresses the wild-type androgen receptor (AR) and which produces the prostate-specific antigen (PSA). In this model, tumors regress soon after castration, but then reproducibly restore their ability to proliferate after 1 to 2 months without AR mutation, mimicking the clinical behavior of CRPC. In the present study, we used this model to identify novel therapeutic targets for CRPC. Evaluating tumor tissues at various stages by gene expression profiling, we discovered that the prostaglandin E receptor EP4 subtype (EP4) was significantly upregulated during progression to castration resistance. Immunohistochemical results of human prostate cancer tissues confirmed that EP4 expression was higher in CRPC compared with hormone-naÃ¯ve prostate cancer. Ectopic overexpression of EP4 in LNCaP cells (LNCaP-EP4 cells) drove proliferation and PSA production in the absence of androgen supplementation in vitro and in vivo. Androgen-independent proliferation of LNCaP-EP4 cells was suppressed when AR expression was attenuated by RNA interference. Treatment of LNCaP-EP4 cells with a specific EP4 antagonist, ONO-AE3-208, decreased intracellular cyclic AMP levels, suppressed PSA production in vitro, and inhibited castration-resistant growth of LNCaP-EP4 or KUCaP-2 tumors in vivo. Our findings reveal that EP4 overexpression, via AR activation, supports an important mechanism for castration-resistant progression of prostate cancer. Furthermore, they prompt further evaluation of EP4 antagonists as a novel therapeutic modality to treat CRPC. 4 samples in each group: androgen-dependent growth (AD), castration-induced regression nadir (ND), and castration-resistant regrowth (CR) stages

2010-06-08 | E-GEOD-21887 | biostudies-arrayexpress

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Identification of EP4 as a Potential Target for the Treatment of Castration-Resistant Prostate Cancer Using a Novel Xenograft Model

Project description:More effective therapeutic approaches for castration-resistant prostate cancer (CRPC) are urgently needed, thus reinforcing the need to understand how prostate tumors progress to castration resistance. We have established a novel mouse xenograft model of prostate cancer, KUCaP-2, which expresses the wild-type androgen receptor (AR) and which produces the prostate-specific antigen (PSA). In this model, tumors regress soon after castration, but then reproducibly restore their ability to proliferate after 1 to 2 months without AR mutation, mimicking the clinical behavior of CRPC. In the present study, we used this model to identify novel therapeutic targets for CRPC. Evaluating tumor tissues at various stages by gene expression profiling, we discovered that the prostaglandin E receptor EP4 subtype (EP4) was significantly upregulated during progression to castration resistance. Immunohistochemical results of human prostate cancer tissues confirmed that EP4 expression was higher in CRPC compared with hormone-naïve prostate cancer. Ectopic overexpression of EP4 in LNCaP cells (LNCaP-EP4 cells) drove proliferation and PSA production in the absence of androgen supplementation in vitro and in vivo. Androgen-independent proliferation of LNCaP-EP4 cells was suppressed when AR expression was attenuated by RNA interference. Treatment of LNCaP-EP4 cells with a specific EP4 antagonist, ONO-AE3-208, decreased intracellular cyclic AMP levels, suppressed PSA production in vitro, and inhibited castration-resistant growth of LNCaP-EP4 or KUCaP-2 tumors in vivo. Our findings reveal that EP4 overexpression, via AR activation, supports an important mechanism for castration-resistant progression of prostate cancer. Furthermore, they prompt further evaluation of EP4 antagonists as a novel therapeutic modality to treat CRPC.

2010-05-19 | GSE21887 | GEO

Gene expression profiling study of VCaP xenograft tumors collected from intact and castrated athymic nude mice

Project description:The purpose of the study was to characterize the properties of human prostate cancer VCaP tumors pre- and post-castration. The main focus was on androgen signaling, androgen metabolism and steroid synthesis. Results provide valuable information about how castration-resistant tumors (CRPC) are able grow in absence of gonadal androgens. One million VCaP cells were inoculated orthotopically into the dorsolateral prostate of nude mice through an abdominal incision. Tumor growth was followed by serum PSA measurements. Intact mice were sacrificed and tumors were collected 3-14 weeks after inoculation (Intact 1, Intact 2). Mice in the remaining three groups (GNX, CRPC 1, CRPC 2) were castrated by removing the testes. Mice were sacrificed and tumors were collected one day after castration (GNX) or 3-14 weeks after castration (CRPC 1, CRPC 2) in castration-resistant stage. 4 tumors were selected from each study group, totally 20 tumors.

2014-04-21 | E-GEOD-56829 | biostudies-arrayexpress

Metabolomics analysis of Vehicle (DMSO/PBS; (1:1) v/v) and DRB18 (10 mg/kg) treated A549 xenograft tumors

Project description:A549 xenograft tumors were treated with (DMSO/PBS; (1:1) v/v) and DRB18 (10 mg/kg) for 5 weeks. The mice were then sacrificed and tumors were then excised. Tumors were then subjected to untargeted metabolomics analysis.

2020-12-07 | ST001638 | MetabolomicsWorkbench

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

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