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Homo sapiens

ABSTRACT: The cistrome of NKX3.1 in LNCaP prostate cancer cells

PROVIDER: PRJNA173399 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR546252.fastq.gz	Fastqsanger.gz
	SRR546253.fastq.gz	Fastqsanger.gz

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The cistrome of NKX3.1 in LNCaP prostate cancer cells

Project description:Here we report the genome-wide set of factors bound by NKX3.1 or control IgG in human prostate cancer cells (LNCaP). Examination of NKX3.1 binding in LNCaP prostate cancer cells

2013-08-21 | E-GEOD-40269 | biostudies-arrayexpress

The cistrome of NKX3.1 in LNCaP prostate cancer cells

Project description:Here we report the genome-wide set of factors bound by NKX3.1 or control IgG in human prostate cancer cells (LNCaP).

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Project description:FOXO4 knockdown in LNCaP prostate cancer cells

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Project description:REST knockdown in LNCaP prostate cancer cells

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Project description:CRISPR screen in LNCaP prostate cancer cells

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FoxA1 specifies unique androgen and glucocorticoid receptor binding events in prostate cancer cells (HTS)

Project description:We report the androgen receptor recruitment to the chromatin of androgen responsive prostate cancer cell lines, LNCaP-1F5 and VCaP in response to physiological androgen 5a-dihydrotestosterone (DHT) using ChIP-sequencing. We compare the AR recruitment by DHT to that by partial agonist/antagonist cyproterone acetate (CPA), mifepristone (RU486) and bicalutamide (Bica) in LNCaP-1F5 cells. We also report the role of glucocorticoid receptor recruitment in presence of dexamethasone (Dex) in androgen responsive prostate cancer cells. The AR and GR cistrome analysis is subsequently compared with gene expression data and RNA Pol II analysis. The ChIP-seq has been performed using AR, GR, RNA Pol II antibodies. Examination of AR and GR binding sites in LNCaP-1F5 and VCaP cells in presence of DHT and Dex respectively. Further analysis of AR binding sites in LNCaP-1F5 cells treated with partial agonist/antagonists, CPA, RU486 and Bica. Additionally RNA Pol II mapping is performed in cells treated with DHT and Dex.

2013-02-05 | E-GEOD-39879 | biostudies-arrayexpress

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Project description:HNRNPL RIP-seq in LNCaP prostate cancer cells

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Project description:50uM Casodex treatment of LNCaP Prostate Cancer cells

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Endogenous androgen receptor proteomic profiling reveals genomic subcomplex involved in prostate tumorigenesis

Project description:Androgen receptor (AR) is a key player in prostate cancer development and progression. Here we applied immunoprecipitation mass spectrometry of endogenous AR in LNCaP cells to identify components of the AR transcriptional complex. In total, 66 known and novel AR interactors were identified in the presence of synthetic androgen, most of which were critical for AR-driven prostate cancer cell proliferation. A subset of AR interactors required for LNCaP proliferation were profiled using chromatin immunoprecipitation assays followed by sequencing, identifying distinct genomic subcomplexes of AR interaction partners. Interestingly, three major subgroups of genomic subcomplexes were identified, where selective gain of function for AR genomic action in tumorigenesis was found, dictated by FOXA1 and HOXB13. In summary, by combining proteomic and genomic approaches we reveal subclasses of AR transcriptional complexes, differentiating normal AR behavior from the oncogenic state. In this process, the expression of AR interactors has key roles by reprogramming the AR cistrome and interactome in a genomic location-specific manner.

2017-10-27 | PXD008056 | Pride

Tumor-Specific Retrogene NANOGP8 Reprograms Prostate Cancer Cells to Castration Resistance by Engaging the FOXA1/AR Signaling Axis and MYC [ChIP-seq]

Project description:Targeted disruption of the embryonic stem cell (ESC) self-renewal and pluripotency factor NANOG has been shown to diminish cancer cell clonogenic growth in vitro and tumor development in vivo. NANOG has also been shown to augment CSC properties and propel the emergence of castration-resistance prostate cancer (CRPC) phenotypes. Here, we investigate the molecular mechanisms underlying NANOG-mediated oncogenesis and prostate cancer progression to androgen independence. ChIP-Seq analysis of LNCaP prostate cancer cells overexpressing doxycycline-inducible NANOG (either NANOG1 or NANOGP8 vs pLVX control) reveal that NANOG coordinately occupies regions of chromatin regulated by AR signaling steroid-receptor complex proteins AR, FOXA1 and NKX3.1. Taken together with the NANOG-induced changes in the prostate cancer transcriptome (RNA-Seq), NANOG appears to reprogram prostate cancer cells to castration resistance by converging on steroid-hormone receptor signaling.

2016-11-08 | GSE74799 | GEO

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