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

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE142195 | 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. [miRNA-Seq]

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

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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.

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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).

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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

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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.

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