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Novel RORg inverse agonists do not modulate androgen receptor activity in prostate cancer

ABSTRACT: Novel RORg inverse agonists do not modulate androgen receptor activity in prostate cancer

PROVIDER: PRJEB29155 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2838520.fastq.gz	Fastqsanger.gz
	ERR2838530.fastq.gz	Fastqsanger.gz
	ERR2838540.fastq.gz	Fastqsanger.gz
	ERR2838521.fastq.gz	Fastqsanger.gz
	ERR2838531.fastq.gz	Fastqsanger.gz

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Novel RORg inverse agonists do not modulate androgen receptor activity in prostate cancer

Project description:Work published by Wang et al. described pharmacological inhibition of RORg with an inverse agonist (SR2211) which led to a decrease in AR gene expression and a reduction in AR protein, which led to the loss of an AR gene expression signature. We have developed a novel, specific, RORg inverse agonist (AZ RORgi) and have studied its effects on the transcriptome of LNCAP cell lines following 24 & 48 hours of treatment. We compare this to SR2211 as well as Enzalutamide, an AR antagonist. We show that Enzalutamide and SR2211 primarily act via the androgen receptor, whereas AZ RORgi does not modulate gene expression in these cell lines.

2019-12-31 | E-MTAB-7294 | biostudies-arrayexpress

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Inverse Agonists of the Androgen Receptor

Project description:We report the efficacy of androgen receptor inverse agonists (ARIAs) in altering androgen receptor (AR) transcriptional activity. Through RNA-sequencing studies in a panel of prostate cancer cell lines and patient derived xenograft models, we demonstrate ARIAs succcessfully inhibit androgen response gene sets. ChIP-seq and CUT&RUN studies demonstrate H3K27ac decreases at AR-target genes in response to treatment. AR and NCOR1/2 localizes at these regions of acetylation loss. HiChIP further revealed loss of 3D connectivity in reponse to ARIA treatment,

2023-06-25 | GSE205980 | GEO

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Project description:Novel RORg inverse agonists do not modulate androgen receptor activity in prostate cancer

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Androgen-sensitive glycomembrane protein expression in LNCaP prostate tumor cells

Project description:Aberrant androgen receptor (AR)-mediated transcription is a critical driver in progression of human prostate cancer. It's known that different doses of androgens can elicit differential transcriptional and proliferative responses in prostate-tumor cells. Here, we set out to examine the androgenic regulation of glycoprotein expression in the membrane fraction of prostate-tumor cells that could serve as mediators or markers of androgen-induced proliferative responses observed in prostate-tumor cells. A bioanalytical workflow involving lectin-affinity chromatography and label-free quantitative mass spectrometry was used to identify androgen-sensitive glycomembrane protein expression associated with androgen-mediated proliferation. This study would facilitate the identification of surface membrane proteins involved in androgen-mediated proliferation and provide potential therapeutic targets in the detection treatment of proliferation prostate-tumors.

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Prostate cancer androgen receptor activity dictates efficacy of bipolar androgen therapy through MYC

Project description:Prostate cancer androgen receptor activity dictates efficacy of bipolar androgen therapy through MYC

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Saracatinib synergizes with enzalutamide to downregulate androgen receptor activity in castration resistant prostate cancer

Project description:We performed RNA-seq to evaluate the consequence of saracatinib's effects on androgen receptor residue Y534 as it pertains to Androgen Receptor gene signatures

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Project description:Androgen receptor (AR) signaling remains the key therapeutic target in the management of hormone-naïve advanced prostate cancer (PCa) and castration-resistant PCa (CRPC). Recently, landmark molecular features have been reported for CRPC, including the expression of constitutively active AR variants that lack the ligand-binding domain. Besides their role in CRPC, AR variants lead to the expression of genes involved in tumor progression. However, little is known about the specificity of their mode of action compared with that of wild-type AR (AR-WT). We performed AR transcriptome analyses in an androgen-dependent PCa cell line as well as cross-analyses with publicly available RNA-seq dataset and established that transcriptional repression capacity that was marked for AR-WT was pathologically lost by AR variants. Functional enrichment analyses allowed us to associate AR-WT repressive function to a panel of genes involved in cell adhesion and epithelial-to-mesenchymal transition. So, we postulate that a less documented AR-WT normal function in prostate epithelial cells could be the repression of a panel of genes linked to cell plasticity, and that this repressive function could be pathologically abrogated by AR variants in PCA.

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