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The estrogen and androgen responses in the immortalized human prostate cancer cell line VCaP

ABSTRACT: The aim of the study was to identify the genes regulated by the estrogen receptor alpha (ERa) in a human prostate cancer cell line (VCaP), with and without the co-activation of the oncogene AR (androgen receptor).

ORGANISM(S): Homo sapiens

PROVIDER: GSE256370 | GEO | 2024/04/19

REPOSITORIES: GEO

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Chromatin targets of androgen receptor and PIAS1 in molecular apocrine breast cancer cells [ChIP-seq]

Project description:The majority of breast cancer subtypes express androgen receptor (AR) in addition to estrogen receptor a (ERa). Depending on the breast cancer subtype androgen signaling has either stimulatory or inhibitory roles in breast cancer cell growth. We have mapped AR cistrome in ERa negative human molecular apocrine breast cancer MDA-MB453 cells and analyzed it in relation to the androgen-regulated transcriptome in the same cells. We have also examined the effect of silencing of the coregulator SUMO ligase PIAS1 on the androgen-regulated transcriptome and AR cistrome in MDA-MB453 cells. Our results show that the MDA-MB453 cells share with VCaP prostate cancer cells a core AR cistrome and target gene signature linked to cancer cell growth and that PIAS1 acts as an AR target gene-selective coregulator in MDA-MB453 cells.

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Project description:Here, we analyze gene expression of prostate cancer cell line VCaP (VCaP WT) and VCaP after testosterone boost (VCaPrev) in order to investigate the impact of the androgen axis on susceptibility to PCA treatments which are not directly AR-directed.

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Single-minded homolog 2 resides in the chromatin protein network of androgen receptor and modulates gene expression in prostate cancer cells Single-minded homolog 2 resides in the chromatin protein network of androgen receptor and modulates gene expression in prostate cancer cells

Project description:We investigated the composition of chromatin protein network around endogenous androgen receptor (AR) in VCaP castration resistant prostate cancer cells using recently developed chromatin-directed proteomic approach called ChIP-SICAP . The androgen-induced AR chromatin protein network contained expected TFs, e.g. HOXB13, chromatin remodeling proteins, e.g. SMARCA4, and several novel candidates not previously associated with AR, e.g. prostate cancer biomarker SIM2. Based on these findings, the role of SMARCA4 and SIM2 was further characterized at AR chromatin domains . Silencing of SIM2 altered chromatin accessibility at a similar number of AR-binding sites as SMARCA4, an established ATPase subunit of the BAF chromatin remodeling complex, often aberrantly expressed in prostate cancer. Despite the wide co-occurrence on chromatin of SMARCA4 and AR, depletion of SMARCA4 influenced chromatin accessibility and expression of a restricted set of AR target genes, in particular those involved in cell morphogenetic changes in epithelial-mesenchymal transition. Silencing of SIM2, in turn, affected the expression of a much larger group of androgen-regulated genes, e.g. those involved in cellular responses to external stimuli and steroid hormone stimulus. The silencing also reduced proliferation of VCaP cells and tumor size in chick embryo chorioallantoic membrane assay, further suggesting the importance of SIM2 in the regulation prostate cancer cells.

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

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Investigation of androgen-regulated lncRNAs in prostate cancer cells

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Human prostate cancer cells (VCaP and AIVCaP): siAR alone (single siRNA) vs. siAR plus OPRK1 (combo-siRNA)

Project description:Through comparative genomics using PDX models of androgen-dependent (AD) and castration-resistant (CR) tumors, we identify opioid receptor kappa 1 (OPRK1) as being associated with castration-resistance. Loss of OPRK1 function delays castration-resistance and inhibits castration-resistant growth of prostate cancer cells in culture and in vivo, suggesting OPRK1 as a therapeutic target. To gain insight with regard to biological function of OPRK1 under androgen-depleted condition, we set up two distinct comparisons using VCaP and AIVCaP cells. AIVCaP is an androgen-independent subline of VCaP which we established. VCaP or AIVCaP were treated with siRNA for AR plus siRNA for OPRK1 (combo-siRNA) or siRNA for AR alone (single siRNA) (n = 4 each), and then expression profile gained from microarray analysis of the respective cell line treated with combo-siRNA was compared with that of cells treated with single siRNA.

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Project description:Androgen receptor (AR) is reactivated in castration resistant prostate cancer (CRPC) through mechanisms including marked increases in AR gene expression. We identify an enhancer in the AR second intron contributing to increased AR expression at low androgen levels in CRPC. Moreover, at increased androgen levels the AR binds this site and represses AR gene expression through recruitment of lysine specific demethylase 1 (LSD1) and H3K4me1,2 demethylation. AR similarly represses expression of multiple genes mediating androgen synthesis, DNA synthesis and proliferation, while stimulating genes mediating lipid and protein biosynthesis. Androgen levels in CRPC appear adequate to stimulate AR activity on enhancer elements, but not on suppressor elements, resulting in increased expression of AR and AR repressed genes that contribute to cellular proliferation. Custom Agilent 44K whole human genome expression oligonucleotide microarrays were used to profile pre-castrated androgen dependent, 4d-post-castrated, and relapsed castration resistant VCaP xenograft tumors in 3 mice. Total RNA was isolated and amplified prior to hybridization against a common reference pool of prostate tumor cell lines.

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