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AR-V7 targets the oncogenic genes in castration resistant prostate cancer.

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE122924 | GEO | 2020/11/02

REPOSITORIES: GEO

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Similar Datasets

AR-V7 targets the oncogenic genes in castration resistant prostate cancer. [ChIP]

Project description:To elucidate the AR-V7 role, we performed ChIP-seq on H3K4me1, H3K4me3, H3K27ac, and AR antibody recognizing the N-terminus of AR and AR splice variants (AR-Vs) using LNCaP and LNCaP95 cells. We showed 399 AR-V7 targeted regions in LNCaP95, most of the AR-V7 target regions could be commonly activated by hormone stimulated AR. However, 22 regions were identified as AR-V7 specific regions. In addition, we show here that AR-V7 can transcript in the ligand independent manner in LNCaP95, unlike LNCaP. We identified the AR-V7 target gene contributing to the CRPC progression.

2020-11-02 | GSE122922 | GEO

AR-V7 targets the oncogenic genes in castration resistant prostate cancer. [RNA]

Project description:To identify the AR-V7 target genes in human prostate cancer, two cell lines (LNCaP, LNCaP95) were subjected to RNA-seq analysis.

2020-11-02 | GSE122923 | GEO

Identification of AR-V7 downstream genes commonly targeted by AR/AR-V7 and specifically targeted by AR-V7 in castration resistant prostate cancer.

Project description:Primary prostate cancer (PC) progresses to castration-resistant PC (CRPC) under androgen deprivation therapy, by mechanisms e.g. expression of androgen receptor (AR) splice variant-7 (AR-V7). Here we conducted comprehensive epigenome and transcriptome analyses comparing LNCaP, primary PC cells, and LNCaP95, AR-V7-expressing CRPC cells derived from LNCaP. Of 399 AR-V7 target regions identified through ChIP-seq analysis, 377 could be commonly targeted by hormone-stimulated AR, and 22 were specifically targeted by AR-V7. Among genes neighboring to these AR-V7 target regions, 78 genes were highly expressed in LNCaP95, while AR-V7 knockdown led to significant repression of these genes and suppression of growth of LNCaP95. Of the 78 AR-V7 target genes, 74 were common AR/AR-V7 target genes and 4 were specific AR-V7 target genes; their most suppressed genes by AR-V7 knockdown were NUP210 and SLC3A2, respectively, and underwent subsequent analyses. NUP210 and SLC3A2 were significantly upregulated in clinical CRPC tissues, and their knockdown resulted in significant suppression of cellular growth of LNCaP95 through apoptosis and growth arrest. Collectively, AR-V7 contributes to CRPC proliferation by activating both common AR/AR-V7 target and specific AR-V7 target, e.g. NUP210 and SLC3A2.

| S-EPMC7581977 | biostudies-literature

AR-V7 targets the oncogenic genes in castration resistant prostate cancer.

Project description:AR-V7 targets the oncogenic genes in castration resistant prostate cancer.

| PRJNA506940 | ENA

AR-V7 Targets in Castration-Resistant Prostate Cancer (CRPC) Cell Line

Project description:In order to define the genes responsible for the growth and survival of a human castration-resistant prostate cancer cell line, a short term (doxycycline inducible) knockdown system was developed and utilized. Three independent 22Rv1 cell isolates were derived for each of the following doxycycline-inducible shRNAs (shGFP, shAR3, and shVav3) (AR3 = AR-V7). The cells were grown in androgen depleted conditions, plus or minus doxycycline, for three days. RNA from the 18 samples was then sent to the University of Miami Genetics Core for RNA Integrity Number (RIN) evaluation and microarray analysis. Genes differentially regulated by AR-V7 knock-down or VAV3 knock-down were explored as downstream targets of AR-V7 or VAV3, respectively.

2018-08-16 | GSE104572 | GEO

AR-V7 targets the oncogenic genes in castration resistant prostate cancer. [RNA]

Project description:AR-V7 targets the oncogenic genes in castration resistant prostate cancer. [RNA]

| PRJNA506948 | ENA

AR-V7 targets the oncogenic genes in castration resistant prostate cancer. [ChIP]

Project description:AR-V7 targets the oncogenic genes in castration resistant prostate cancer. [ChIP]

| PRJNA506945 | ENA

Androgen Receptor splice variant V7 (AR-V7) mediates AR signalling in castration resistant prostate cancer (CRPC)

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-01-21 | GSE143907 | GEO

Diverse AR-V7 cistromes in castration-resistant prostate cancer are governed by HoxB13.

Project description:The constitutively active androgen receptor (AR) splice variant 7 (AR-V7) plays an important role in the progression of castration-resistant prostate cancer (CRPC). Although biomarker studies established the role of AR-V7 in resistance to AR-targeting therapies, how AR-V7 mediates genomic functions in CRPC remains largely unknown. Using a ChIP-exo approach, we show AR-V7 binds to distinct genomic regions and recognizes a full-length androgen-responsive element in CRPC cells and patient tissues. Remarkably, we find dramatic differences in AR-V7 cistromes across diverse CRPC cells and patient tissues, regulating different target gene sets involved in CRPC progression. Surprisingly, we discover that HoxB13 is universally required for and colocalizes with AR-V7 binding to open chromatin across CRPC genomes. HoxB13 pioneers AR-V7 binding through direct physical interaction, and collaborates with AR-V7 to up-regulate target oncogenes. Transcriptional coregulation by HoxB13 and AR-V7 was further supported by their coexpression in tumors and circulating tumor cells from CRPC patients. Importantly, HoxB13 silencing significantly decreases CRPC growth through inhibition of AR-V7 oncogenic function. These results identify HoxB13 as a pivotal upstream regulator of AR-V7-driven transcriptomes that are often cell context-dependent in CRPC, suggesting that HoxB13 may serve as a therapeutic target for AR-V7-driven prostate tumors.

| S-EPMC6042123 | biostudies-literature

Clinical Utility of CLIA-Grade AR-V7 Testing in Patients With Metastatic Castration-Resistant Prostate Cancer.

Project description:A splice variant of the androgen receptor, AR-V7, confers resistance to AR-targeted therapies (ATTs) but not taxane chemotherapies in patients with metastatic castration-resistant prostate cancer. Since August 2015, a clinical-grade assay to detect AR-V7 messenger RNA expression in circulating tumors cells (CTCs) has been available to providers through a Clinical Laboratory Improvement Amendments-certified laboratory at Johns Hopkins University.We contacted ordering providers of the first 150 consecutive tests by using a questionnaire-based survey to determine how the results of AR-V7 testing were used to influence clinical practice.In all, 142 (95%) of 150 questionnaires were completed by 38 providers from 29 sites across the United States and Canada. AR-V7 test results were reported either as CTC- (28%), CTC+/AR-V7- (30%), or CTC+/AR-V7+ (42%). Prevalence of AR-V7 detection increased with prior exposure to ATTs (abiraterone and enzalutamide naïve, 22%; after abiraterone or enzalutamide, 35%; after abiraterone and enzalutamide, 43%). Overall, management was affected by AR-V7 testing in 53% of the patients and even more often with CTC+/AR-V7+ results. AR-V7+ patients were commonly switched from ATT to taxane chemotherapy (43%) or were offered a clinical trial (43%); management remained unchanged in only 14% of these patients. Overall, patients who had a change in management on the basis of AR-V7 testing were significantly more likely to achieve a physician-reported 50% decline in prostate-specific antigen response on next-line therapy than those who did not change treatment (54% v 31%; P = .015).Providers used AR-V7 testing to influence clinical decision making more often than not. Physicians reported thatmenwithAR-V7+results had the most treatment changes, and such men were preferentially managed with taxane therapy or offered a clinical trial, which may have improved outcomes.

| S-EPMC5697780 | biostudies-other

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