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Potent stimulation of the androgen receptor instigates a viral mimicry response in prostate cancer [RNA-seq]

ABSTRACT: Potent stimulation of the androgen receptor instigates a viral mimicry response in prostate cancer [RNA-seq]

PROVIDER: PRJNA777549 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16761405_1.fastq.gz	Fastqsanger.gz
	SRR16761405_2.fastq.gz	Fastqsanger.gz
	SRR16761406_1.fastq.gz	Fastqsanger.gz
	SRR16761406_2.fastq.gz	Fastqsanger.gz
	SRR16761407_1.fastq.gz	Fastqsanger.gz

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Potent stimulation of the androgen receptor instigates a viral mimicry response in prostate cancer

Project description:Potent stimulation of the androgen receptor instigates a viral mimicry response in prostate cancer

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Potent stimulation of the androgen receptor instigates a viral mimicry response in prostate cancer [ChIP-seq]

Project description:Potent stimulation of the androgen receptor instigates a viral mimicry response in prostate cancer [ChIP-seq]

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Potent stimulation of the androgen receptor instigates a viral mimicry response in prostate cancer [ChIP-seq]

Project description:Inhibiting the androgen receptor (AR), a ligand-activated transcription factor, with androgen deprivation therapy is a standard-of-care treatment for metastatic prostate cancer (PCa). Paradoxically, activation of AR can also inhibit the growth of PCa in some patients and experimental systems, but the mechanisms underlying this phenomenon are poorly understood. This study exploited a potent synthetic androgen, methyltestosterone (MeT), to investigate AR agonist-induced growth inhibition. MeT strongly inhibited growth of PCa cells expressing AR, but not AR-negative models. Genes and pathways regulated by MeT were highly analogous to those regulated by DHT, although MeT induced a quantitatively greater androgenic response in PCa cells. MeT potently down-regulated DNA methyltransferases, leading to global DNA hypomethylation. These epigenomic changes were associated with dysregulation of transposable element expression, with long-term MeT treatment resulting in upregulation of endogenous retrovirus (ERV) transcripts. Increased ERV expression led to accumulation of double-stranded RNA and a “viral mimicry” response characterised by activation of interferon signalling, upregulation of MHC Class I molecules and enhanced recognition of murine PCa cells by CD8+ T cells. Positive associations between AR activity and ERVs/anti-viral pathways were evident in patient transcriptomic data, supporting the clinical relevance of our findings. Collectively, our study reveals that the potent androgen MeT can increase the immunogenicity of PCa cells via a viral mimicry response, a finding that has potential implications for the development of strategies to sensitize this cancer type to immunotherapies.

2022-02-01 | GSE188150 | GEO

Potent stimulation of the androgen receptor instigates a viral mimicry response in prostate cancer [RNA-seq]

2022-02-01 | GSE187413 | GEO

Potent stimulation of the androgen receptor instigates a viral mimicry response in prostate cancer

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

2022-02-01 | GSE187414 | GEO

Epigenomic and transcriptomic profiles a of prostate cancer cell line with and without androgen stimulation

Project description:We performed H3K27ac ChIP-seq, ATAC-seq, and RNA-seq in LNCaP with and without androgen stimulation

2022-06-14 | GSE205885 | GEO

Androgen stimulation time-course of TMPRSS2-ERG fusion positive VCaP cells.

Project description:The TMPRSS2-ERG fusion positive prostate cancer cell line VCaP was grown for 72h in steroid depleted media (RPMI 10% CDT FBS) prior to vehicle (ethanol) or androgen stimulation (1nM R1881). To allow detailed analysis of androgen regulated gene expression in the VCaP prostate cancer cell line total RNA was harvested every every hour up to 24h using trizol (Sigma), quantified using a Nanodrop spectrophotometer (ND-1000). RNA samples were prepared for analysis on Illumina Human 12 v3 BeadArrays. Raw bead-summary data were generated using GenomeStudio version 1.9.0 (Illumina Inc.). For integrative analysis expression array data were normalised in R using the beadarray software and BASH (see Supplementary Methods for details) (Cairns et al., 2008; Dunning et al., 2007).

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Transcriptome changes upon androgen deprivation and DHT stimulation in LNCaP cells

Project description:Transcriptome changes upon androgen deprivation and DHT stimulation in LNCaP cells

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Androgen receptor cistrome in breast cancer cell line MDA-MB-453 with 5a-dihydrotestosterone (DHT) stimulation

Project description:Androgen receptor (AR) is expressed in 60-70% of breast cancers independent of estrogen receptor (ER) expression, however its function in breast cancer is largely unknown. Our study identified the high level of AR in ERâ??/HER2+ breast tumors and andorgen and AR greatly stimulated growth of MDA-MB-453 breast cancer cells. To define the genome-wide AR binding sites, we performed AR ChIP-seq using MDA-MB-453 breast cancer cells followig stimulation of DHT. We also identified FOXA1 is a crucial AR cofactor in MDA-MB-453 cells and the FOXA cistrome showed signaficant overlap with AR at both early and late time points of DHT stimulation. AR ChIP was performed in MDA-MB-453 breast cancer cells following 5a-dihydrotestosterone (DHT) stimulation for 4h and 16h respectively. FOXA1 ChIP-seq was performed after 4h DHT stimulation in MDA-MB-453 cells.

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Gene expression of osteosarcama cell line with vasculogenic mimicry phenotype

Project description:Vasculogenic mimicry has been generally accepted as a new form of tumor vascularization and regarded as an unfavorable prognostic factor in multiple aggressive malignancies. We previously reported the presence of vasculogenic mimicry in osteosarcoma patients. The mechanistic basis for osteosarcoma VM remains unclear. We used microarrays to detail the global programme of gene expression between 143B cells and HOS cells exposed to Matrigel which showed greatly different vasculogenic mimicry formation potential and identified distinct classes of vasculogenic mimicry-realted genes during this process.

2018-09-15 | GSE119975 | GEO

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