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

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

PROVIDER: PRJNA506948 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8242650.fastq.gz	Fastqsanger.gz
	SRR8242660.fastq.gz	Fastqsanger.gz
	SRR8242651.fastq.gz	Fastqsanger.gz
	SRR8242661.fastq.gz	Fastqsanger.gz
	SRR8242652.fastq.gz	Fastqsanger.gz

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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.

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. [ChIP]

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

| PRJNA506945 | ENA

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.

2018-05-31 | GSE99378 | 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

Transcriptional profiles of castration resistant prostate cancer cells treated with ITRI-148 PROTAC targeting AR and AR-V7

Project description:Androgen receptor (AR) signaling remains a key driver of castration-resistant prostate cancer, with AR splice variants like AR-V7 mediating resistance to second-generation antiandrogens. Targeting the AR N-terminal domain (NTD) offers a strategy to bypass ligand-binding domain-mediated resistance. We developed a VHL-based (ITRI-90) and a CRBN-based (ITRI-148) PROTAC degrader capable of targeting AR and AR-V7 via NTD. These compounds demonstrate potent antitumor activity towards castration-resistant and enzalutamide resistant xenograft models. Transcriptomic analyses confirm robust suppression of AR and AR-V7 target genes by ITRI-148 in VCaP cells. The transcriptomic effects of these AR-NTD degraders in enzalutamide-resistant C4-2B/MDVR cells closely mirror that of AR knockdown.

2025-11-13 | GSE297577 | GEO

Transcriptome profiling of castration-resistant prostate cancer cells treated with novel androgen receptor (AR) and AR-V7 inhibitors

Project description:The purpose of this study was to characterize the downstream transcriptomic effects of ARVib-mediated degradation of AR/AR-V7, particularly in attenuating AR/AR-V7 target gene expression in prostate cancer cells. Towards this goal, next-generation sequencing (NGS)-based gene expression profiling (RNA-Sequencing; RNA-Seq) was performed on castration-resistant prostate cancer (CRPC) C4-2B MDVR cells that were treated with vehicle control or one of the AR/AR-V7 inhibitors (ARVib), ARVib-7 or ARVib-31.

2021-08-22 | GSE158556 | GEO

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

Project description:CRPC remains AR dependent. There are multiple mechanisms for reactivation of AR including expression of constitutively active AR splices variant AR-V7 (AR3). Earlier studies suggest that though the variants regulate many of the same genes as AR, they also have unique targets. Another argument is that the variant is a “weak” AR. We have used an LNCaP cell line that expresses AR-V7 in response to doxycycline (LNCaP AR-V7) to compare the activities of the two isoforms and to identify differential regulation of target genes. We also used VCaP cell line that expresses AR-V7 in response to doxycycline (VCaP AR-V7) to validate the activities of the two isoforms in an alternative prostate cancer cell line. The transcriptomes for AR and AR-V7 in these cell lines were identified using RNA-Seq.

2021-01-21 | GSE143905 | GEO

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

Project description:CRPC remains AR dependent. There are multiple mechanisms for reactivation of AR including expression of constitutively active AR splices variant AR-V7 (AR3). Earlier studies suggest that though the variants regulate many of the same genes as AR, they also have unique targets. Another argument is that the variant is a “weak” AR. We have used an LNCaP cell line that expresses AR-V7 in response to doxycycline to compare DNA interactions of the two isoforms and to identify differential regulation of target genes. ChIP-exo method was used to map AR and AR-V7 interaction with DNA in LNCaP engineered cell line (LNCaP AR-V7) at single base resolution.

2021-07-07 | GSE143906 | GEO

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