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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

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

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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.

2024-02-21 | GSE142196 | GEO

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Project description:G-1 is an agonist to GPR30. Activation of GPR30 by G-1 inhibited prostate cancer cell growth in LNCaP xenografts regrown after catration of the host (nude mice), but not in the androgen-sensitive LNCaP xenograft grown in an intact host. Results provide insights into the molecular basis of G-1 action in castration-resistant prostate cancer. Male nude mice were injected with LNCaP cells. When the LNCaP tumors reached 150–300 mm3, mice were divided into two groups: intact (androgen-sensitive tumor) and castrated. For the intact group, mice were subcutaneously injected with vehicle alone (95% PBS, 2.5% DMSO, 2.5% ethanol) or G-1 (4 mg/kg/day in vehicle) daily for 16 days. For the castrated group, tumors regressed and then regrew to ~300-400mm3. Mice were treated daily with vehicle or G-1 as described for 16 days. Tumors were harvested for RNA extraction and microarray experiments.

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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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