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Inhibition of nucleotide biosynthesis to enhance responses to drugs targeting androgen biosynthesis and the androgen receptor. [miRNA-Seq]

ABSTRACT: RNA-Seq (miRNA) analysis of prostate cancer cells derived from xenografts treated daily with drugs targeting androgen biosynthesis and the androgen receptor.

ORGANISM(S): Homo sapiens

PROVIDER: GSE142193 | GEO | 2024/02/21

REPOSITORIES: GEO

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Inhibition of nucleotide biosynthesis to enhance responses to drugs targeting androgen biosynthesis and the androgen receptor. [RNA-Seq]

Project description:RNA-Seq analysis of prostate cancer cells derived from xenografts treated daily with drugs targeting androgen biosynthesis and the androgen receptor.

2024-02-21 | GSE142195 | GEO

Inhibition of nucleotide biosynthesis to enhance responses to drugs targeting androgen biosynthesis and the androgen receptor

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

2024-02-21 | GSE142196 | GEO

LNCAP in-vitro treatment with androgen receptor targeting drugs

Project description:Gene expression in LNCaP cells after treatment with the androgen receptor targeting drugs bicalutamide (BIC), enzalutamide (ENZ) and apalutamide (ARN) in the presence or absence of dihydrotestosterone (DHT).

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The effect of GPR30 agonist G-1 on androgen-sensitive and castration-resistant LNCaP xenografts

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2014-02-14 | E-GEOD-54974 | biostudies-arrayexpress

Regulators of Human Androgen Biosynthesis

Project description:Androgens are essential for sexual development and reproduction. However, androgen regulation in health and disease is poorly understood. Previously, we showed that human adrenocortical H295R cells grown under starvation conditions acquire a hyperandrogenic steroid profile with changes in steroid metabolizing enzymes HSD3B2 and CYP17A1 essential for androgen production. Furthermore, we have shown that metformin inhibits androgen production of steroidogenic H295R cells and inhibits complex I activity of the respriatory chain. Therefore, to search for underlying mechanisms regulting androgen production and to understand the basic biology of androgens, we have characterized the gene expression profile of H295R cells grown under normal growth conditions, serum starvation (hyperandrogenic) growth conditions as well as after metformin treatment (hypoandrogenic). In this dataset, we first characterized the gene expression profile of H295R cells cultured under nromal growth vs serum-starved (hypernadrogenic) growth conditions. Expression profiling of starved H295R cells revealed alterations in genes involved in steroid and energy metabolism and signal transduction. We discovered two new gene networks around RARB and ANGPTL1, and show how they regulate androgen biosynthesis (Udhane SS et al.,2015). In a second part, we compared the gene expression profile of H295R cells grown under serum starvation (hyperandrogenic) conditions to metformin treated (hypoandrogenic) cells in search for the underlying androgen regulating network. (Udhane et al., manuscript in preparation).

2018-01-01 | GSE88795 | GEO

The effect of androgen deprivation on human prostate xenograft tumor LuCaP35

Project description:Androgen deprivation is a standard of care front-line therapy for human prostate cancer, however, majority of patients will eventally develop resistance to androgen deprivation. In this study, using a human prostate cancer xenograft model -LuCaP35, we examiend the gene expression changes after castration. We compare the gene expression of 5 LuCaP35 xenografts from non-treated mice (Control), and 5 androgen-deprived LuCaP35 xenografts from castrated mice (Castration).

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Development of an Androgen Receptor Inhibitor Targeting the N-Terminal Domain of Androgen Receptor for Treatment of Castration Resistant Prostate Cancer

Project description:Prostate cancer patients undergoing androgen deprivation therapy almost invariably develop castration-resistant prostate cancer. Resistance occurs when mutations in the androgen receptor (AR) render anti-androgen drugs ineffective or when constitutively active splice variants lacking the androgen binding domain entirely (e.g. ARV7) is expressed. In this study, we are reporting the discovery of novel AR-NTD covalent inhibitor 1‐chloro‐3‐[(5‐([(2S)‐3‐chloro‐2‐hydroxypropyl]amino)naphthalen‐1‐yl)amino]propan‐2‐ol (VPC-220010) targeting the AR-N-terminal Domain (AR-NTD). VPC-220010 inhibits AR-mediated transcription of full length and truncated variant ARV7, downregulates AR response genes, and selectively reduces the growth of both full-length AR- and truncated AR-dependent prostate cancer cell lines. We show that VPC-220010 disrupts interactions between AR and its known coactivators and interactors, such as CHD4, FOXA1, ZMIZ1, and several SWI/SNF complex proteins. Taken together, our data suggest that VPC-220010 is a promising small molecule AR-NTD inhibitor for the treatment of CRPC.

2021-07-28 | GSE173331 | GEO

A combinatorial screen of the CLOUD uncovers a synergy targeting the androgen receptor

Project description:Approved drugs are invaluable tools to study biochemical pathways and further characterization of these compounds may lead to repurposing of single drugs or combinations. Here, we describe a collection of 308 small molecules representing the diversity of structures and molecular targets of all FDA-approved chemical entities. The CeMM Library of Unique Drugs (CLOUD) covers prodrugs and active forms at pharmacologically relevant concentrations and is ideally suited for combinatorial studies. We screened pairwise combinations of CLOUD drugs for impairment of cancer cell viability and discovered the synergistic interaction between flutamide and phenprocoumon (PPC). The combination of these two drugs modulates the stability of the androgen receptor (AR) and resensitizes AR mutant prostate cancer cells to flutamide. Mechanistically, we show that the AR is a substrate for γ-carboxylation, a post-translational modification inhibited by PPC. Collectively, our data suggest that PPC might be repurposed to tackle resistance to antiandrogens in prostate cancer patients.

2017-03-06 | GSE94783 | GEO

Effects of small molecules targeting the androgen receptor DNA-binding domain on prostate cancer cell transcriptome

Project description:Prostate cancer is a leading cause of cancer related death among men. Current Androgen Receptor (AR) antagonists often target the ligand binding domain (LBD). However, occurrence of resistance to drugs targeting the LBD is common due to emergence of mutations in the LBD or constitutively active variants that lack the LBD itself. Two novel small molecules, VPC-17005 and VPC-14449 targeting the DNA-binding domain have been developed and published previously. In this study, LNCaP cells were treated with one of these drugs or the well-established AR antagonist Enzalutamide, and the transcriptomic changes have been determined using RNA-seq analysis.

2019-07-20 | GSE127816 | GEO

Targeting the N-terminus of the androgen receptor for prostate cancer therapy

Project description:All current clinically approved androgen deprivation therapies for prostate cancer (PCa) target the C-terminal ligand-binding domain (LBD) of the androgen receptor (AR), although the N-terminal domain (NTD) is the main regulator of AR activity. Targeting the AR NTD directly is a challenge because of its intrinsic disordered nature and the lack of secondary structure and clefts for drugs to bind. Here, we make use of the cochaperone BAG1L that functions through the NTD to develop alternative AR inhibitors. We show that BAG1L binds to a short alpha-helical region of the AR NTD and regulates AR dynamics and the expression of AR target genes. We further show that disruption of the BAG1L-AR NTD action by a small molecule 2-(4-fluorophenyl)-5-(trifluoromethyl)-1,3-benzothiazole (A4B17) downregulates AR target gene expression and blocks proliferation of AR-positive PCa cells. Targeting a cochaperone as a surrogate to the AR NTD is therefore key to developing novel AR antagonists.

2021-07-01 | GSE159606 | GEO

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