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KIF15 confers resistance to enzalutamide in castration resistant prostate cancer [RNA-Seq]

ABSTRACT: The aim of this research was to confirm the regulatory effect of KIF15 on gene expression in castration resistant prostate cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE150895 | GEO | 2021/05/20

REPOSITORIES: GEO

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KIF15 confers resistance to enzalutamide in castration resistant prostate cancer [array]

Project description:The aim of this research was to confirm the regulatory effect of KIF15 on gene expression in castration resistant prostate cancer.

2021-05-20 | GSE146984 | GEO

RUVBL1 promotes enzalutamide resistance of prostate tumors through the PLXNA1-CRAF-MAPK pathway

Project description:The aim of this research was to confirm the regulatory effect of RUVBL1 on gene expression in castration resistant prostate cancer.

2022-03-02 | GSE197630 | GEO

KIF15 confers resistance to enzalutamide in castration resistant prostate cancer [array]

Project description:KIF15 confers resistance to enzalutamide in castration resistant prostate cancer [array]

| PRJNA612624 | ENA

KIF15 confers resistance to enzalutamide in castration resistant prostate cancer [RNA-Seq]

Project description:KIF15 confers resistance to enzalutamide in castration resistant prostate cancer [RNA-Seq]

| PRJNA634007 | ENA

Targeting Electron Transport Chain Confers Therapeutic Vulnerability in Castration-Resistant Prostate Cancer

Project description:Most prostate cancer will develop into castration-resistant prostate cancer, which is the most frequent cause of death for prostate cancer patients. Despite novel androgen receptor antagonists have significantly improved clinical outcomes for these patients, some patients still could not benefit from existing treatment regimens. By analyzing the single-cell RNA-sequencing data and bulk-sequencing data, we discovered that oxidative phosphorylation and electron transport chain (ETC) pathway were enhanced in the prostate cancer microenvironment following tumor progression. Meanwhile, high ETC was related to poor clinical outcomes in prostate cancer patients. Both in vitro and in vivo castration-resistant prostate cancer models demonstrated that ETC inhibitor marked suppressed tumor growth and the synergistic antitumor efficacy of the combination of ETC inhibitor and androgen receptor antagonist. Our study indicates that ETC activity is a metabolic vulnerability for advanced prostate cancer and can serve as a novel therapeutic target.

2023-01-15 | GSE206962 | GEO

A Novel Peptide Encoded by circSRCAP Confers Resistance to Enzalutamide by Inhibiting the Ubiquitin-Dependent Degradation of AR-V7 in Castration-Resistant Prostate Cancer

Project description:Background: The sustained activation of androgen receptor splice variant-7 (AR-V7) is a key factor in the resistance of castration-resistant prostate cancer (CRPC) patients to second-generation anti-androgen (AR) drugs such as enzalutamide (ENZ). The AR/AR-V7 protein is regulated by the E3 ubiquitin ligase STUB1 and a protein complex formed by HSP70. However, the specific mechanism remains elusive. Methods: High-throughput RNA sequencing was employed to detect differentially expressed circular RNAs (circRNAs) in ENZ-resistant and control CRPC cells. The coding potential of circSRCAP was identified through polysome profiling and LC-MS. The function of circSRCAP was validated in vitro and in vivo via gain or loss of function assays. Mechanistic insights were derived from immunoprecipitation analyses. Results: A novel ENZ-resistant circular RNA (circRNA) named circSRCAP has been identified, showing upregulation in ENZ-resistant C4-2B cells (ENZR-C4-2B) and correlation with elevated protein levels of AR-V7. circSRCAP undergoes cleavage into a loop by the splicing factor EIF4A3 and is derived from the nucleus by the RNA helicase DDX39A. Mechanistically, circSRCAP encodes a 75 amino acid peptide, circSRCAP-75aa, which inhibits the ubiquitination of the AR/AR-V7's co-chaperone protein HSP70 by dissociating STUB1, a ubiquitin E3 ligase. This process leads to the upregulation of AR-V7 protein expression, thereby promoting resistance of castration-resistant prostate cancer (CRPC) cells to ENZ. Xenograft tumor models further confirm the role of circSRCAP in CRPC progression and its potential as a therapeutic target for ENZ-resistant CRPC (ENZR-CRPC). Conclusions: circSRCAP presents an epigenetic mechanism that sheds light on the fate determination of AR-V7, offering a promising therapeutic target for the treatment of ENZR-CRPC.

2025-01-29 | GSE264133 | GEO

Androgen receptor splice variants mediate enzalutamide resistance in castration-resistant prostate cancer cell lines

Project description:The goal of this experiment was to compare the gene expression programs mediated by androgen/AR vs. constitutively active, truncated AR variants in castration-resistant CWR-R1 prostate cancer cells. Because constitutive activity of truncated AR variants can mask androgen/AR target genes, the androgen/AR transcriptional program was assessed by silencing the trucnated AR 1/2/3/CE3 variant with siRNA targeting AR exon CE3 and treating cells with vehicle (ethanol) or 1nM DHT. Similarly, because full-length AR activity can mask truncated AR variant target genes, the AR variant transcriptional program was assessed under castrate conditions by selectively silencing full-length AR with siRNA targeting AR exon 7, and comparing this profile with CWR-R1 cells transfected wtih siRNA targeting AR exon 1, which silences all AR expression (full-length and truncated AR variants). CWR-R1 cells were maintained under castrate conditions in long term culture in order to enrich for the population of cells harboring a 48kb intragenic deletion in AR intron 1. These late-passage CWR-R1 cells were electroporated with siRNAs targeting AR exon 1, AR exon 7, or AR exon CE3. Electroporated cells were seeded in RPMI 1640 medium containing antibiotics and 5% charcoal-stripped, steroid-depleted medium and allowed to recover for 48h. After this 48h recovery, electroporated cells were switched to serum-free RPMI 1640 with 1nM DHT or 0.1% ethanol (vehicle control) for an additional 24h prior to extraction of total RNA. Three independent biological replicates were performed.

2012-10-23 | E-GEOD-41784 | biostudies-arrayexpress

Proteome profiling of enzalutamide-resistant cell lines and serum analysis identified ALCAM as marker of resistance in castration-resistant prostate cancer

Project description:Enzalutamide (ENZA) is a frequently used therapy in metastatic castration-resistant prostate cancer (mCRPC). Baseline or acquired resistance to ENZA have been observed, but the molecular mechanisms of resistance are poorly understood. We aimed to identify proteins involved in ENZA resistance and to find therapy-predictive serum markers. We performed comparative proteome analyses on ENZA-sensitive parental (LAPC4, DUCAP) and -resistant prostate cancer cell lines (LAPC4-ENZA, DUCAP-ENZA) using liquid chromatography tandem mass spectrometry (LC-MS/MS). The most promising 4 marker candidates were selected using bioinformatic approaches. Serum concentrations of selected markers (ALCAM, AGR2, NDRG1, IDH1) were measured in 72 ENZA-treated mCRPC patients’ samples using ELISA. In addition, ALCAM serum levels were measured in 101 Abiraterone (ABI) and 100 Docetaxel (DOC)-treated mCRPC patients. Results were correlated with clinical and follow-up data. The functional role of ALCAM in ENZA resistance was assessed in vitro using siRNA. Our proteome analyses revealed 731 significantly differentially abundant proteins between ENZA-sensitive and -resistant cells and our filtering methods identified 4 biomarker candidates. Serum analyses of these proteins revealed only ALCAM to be associated with poor patient survival. Furthermore, higher baseline ALCAM levels were associated with poor survival in ABI- but not in DOC-treated patients. In LAPC4-ENZA resistant cells, ALCAM silencing by siRNA knockdown resulted in significantly enhanced ENZA sensitivity. Our analyses revealed that ALCAM serum levels may help to identify ENZA- and ABI-resistant patients and may thereby help to optimize future clinical decision-making. Our functional analyses suggest the possible involvement of ALCAM in ENZA resistance.

2022-06-24 | PXD031847 | Pride

Androgen receptor splice variants mediate enzalutamide resistance in castration-resistant prostate cancer cell lines

2012-10-23 | GSE41784 | GEO

Androgen receptor gene aberrations in circulating cell-free DNA: biomarkers of therapeutic resistance and response in castration-resistant prostate cancer

Project description:aCGH experiment on cell-free DNA collected from the plasma of patients with castration-resistant prostate cancer. No replicates. castration-resistant prostate cancer vs male reference DNA

2015-03-09 | E-GEOD-61134 | biostudies-arrayexpress

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