Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Regulators of Human Androgen Biosynthesis

ABSTRACT: 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).

ORGANISM(S): Homo sapiens

PROVIDER: GSE88795 | GEO | 2018/01/01

SECONDARY ACCESSION(S): PRJNA348635

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

An integrated RNA-Seq and network study reveals the effect of nicotinamide on adrenal androgen synthesis

Project description:Acne vulgaris is a chronic inflammatory disease of the skin resulting from androgeninduced increased sebum production and altered keratinization. Nicotinamide (NAM), an amide form of vitamin B3 with a well-established safety profile, has shown good therapeutic potential in treating acne and its complications. NAM has anti-inflammatory effects and reduces sebum but its function in androgen biosynthesis remains unknown. In this study, we used a widely used cell model, starved human adrenal NCI-H295R cells, to examine the effects of NAM in androgen production and its mediated network changes. By treating NCI-H295R cells with 1-25 mmol/L of NAM, we found that cell viability was only slightly inhibited at the highest dose (25 mmol/L). NAM reduced testosterone production in a dose-dependent manner. Transcriptomic analysis demonstrated that key enzymes of androgen biosynthesis were significantly decreased under NAM treatment. In addition, gene set enrichment analysis (GSEA) showed that gene sets of cell cycle, steroid biosynthesis, TGFβ signalling, and targets of IGF1 or IGF2 were enriched in NAM-treated cells. Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathway and Gene ontology (GO) analysis of the differentially expressed genes also suggested that steroidogenesis and SMAD signalling were affected by NAM. Overall, these crucial genes and pathways might form a complex network in NAM-treated NCI-H295R cells and result in androgen reduction. These findings help explain the potential molecular actions of NAM in acne vulgaris, and position NAM as a candidate for the treatment of other hyperandrogenic disorders.

2020-11-19 | GSE161730 | GEO

Genome-wide analysis of serum starved prelamin A-accumulating hMSCs gene expression.

2014-06-23 | GSE52563 | GEO

Human microRNA (miRNA) expression during serum starvation

Project description:The study aimed to identify the differentially regulated microRNAs during serum starvation. We identified miRNAs exhibiting altered expression in asynchronous, serum starved and serum re-supplemented human cells. We identified several miRNAs that were upregulated following serum starvation and downregulated upon serum re-supplementation.

2017-09-05 | GSE103436 | GEO

RNA-seq profiling identifies Androgen Receptor-regulated genes in prostate cancer cells

Project description:The goal of this analysis is to profile AR-regulated genes, especially non-coding RNAs in three androgen sensitive prostate cancer cell lines, MDA-PCA-2B, LNCaP and VCaP. The two cell lines were serum-starved first, followed by dihydrotestosterone (DHT) stimulation or treated with Enzalutamide (AR inhibitor) without starvation. Transcriptome profiling was generated by RNA-sequencing from polyA-selected RNA. These experiments are followed by knock-down experiments of AR and ARlnc1 in MDA-PCA-2B, and also Enzalutamide (anti-androgen) treatment of LNCaP cells.

2018-02-21 | GSE110903 | GEO

Genome-wide analysis of serum starved prelamin A-accumulating hMSCs gene expression.

Project description:Analysis of serum starved prelamin A-accumulating hMSCs at gene expression level. The hypothesis tested in the present study was that prelamin A accumulation induces the dysregulation of genes that are essensial for cell survival under a stress condition such as serum starvation. The results provide important information about these genes and the functional categories that are dysregulated due to prelamin A accumulation in serum starved hMSCs. Two samples are analyzed in this microarray experiment: human mesenchymal stem cell cultured under serum starvation conditions (during 24 hours) which accumulate prelamin A (pre-hMSCs) and control mesenchymal stem cells (ctrl-hMSCs). 2 biological replicates (hMSCs derived from 2 different bone marrow donors) and 1 technical replicate are included in this analysis.

2014-06-23 | E-GEOD-52563 | biostudies-arrayexpress

Identification of drivers and therapeutic vulnerabilities in anti-androgen resistant prostate cancer cells

Project description:Inhibition of the androgen receptor (AR) by anti-androgens is the standard treatment for castration resistant prostate cancer (CRPC), but it inevitably leads to the development of resistance. We generated two multi anti-androgen resistant cell-line models by treatment of LNCaP cells with enzalutamide (ResA) and RD-162 (ResB). Both cell-lines have an AR independent, non-neuroendocrine phenotype. To identify the resistance mechanisms we performed RNASeq analysis. To this end, the three cell-lines were plated in medium with 5% dextran-coated charcoal (DCC) treated FCS at a density of 1 million cells/well in 6-well plates. After 24 hours of steroid starvation the cells were treated with 10 nM of the androgen dihydrotestosterone (DHT), 10 µM of the anti-androgen enzalutamide, a combination of the two, or vehicle (DMSO) for 18 hours.

2019-09-26 | GSE130534 | GEO

Gene expression profiling study of VCaP xenograft tumors collected from intact and castrated athymic nude mice

2014-04-21 | GSE56829 | GEO

ChIP-seq of the androgen receptor (AR) in MDAMB453 cells after androgen stimulation

Project description:Serum starved MDAMB453 cells were serum starved and treated for 4 hours with vehicle control (ethanol), 5α-dihydrotestosterone (DHT; 10nM) or medroxyprogesterone acetate (MPA; 10nM). AR binidng peaks were determined. Subsequent analysis showed that binding sites for androgen receptor are enriched at breast cancer risk loci.

2015-10-16 | GSE74069 | GEO

Effects of novel antiandrogens (enzalutamide and ARN-509) on global gene expression in castration-resistant prostate cancer (CRPC) xenograft model

Project description:Global transcriptome analysis revealed altered expression of 291 genes, including mRNAs for several AR-interacting proteins and multiple enzymes involved in steroid metabolism. The data indicate that antiandrogens modify the androgen signaling in VCaP xenografts at multiple levels by reducing concentrations of active androgens, increasing AR expression and inducing alterations in the expression of AR interacting proteins, steroid metabolizing enzymes and AR downstream target genes.

2017-10-09 | GSE95413 | GEO

Gene expression profiling study of VCaP xenograft tumors collected from intact and castrated athymic nude mice

Project description:The purpose of the study was to characterize the properties of human prostate cancer VCaP tumors pre- and post-castration. The main focus was on androgen signaling, androgen metabolism and steroid synthesis. Results provide valuable information about how castration-resistant tumors (CRPC) are able grow in absence of gonadal androgens. One million VCaP cells were inoculated orthotopically into the dorsolateral prostate of nude mice through an abdominal incision. Tumor growth was followed by serum PSA measurements. Intact mice were sacrificed and tumors were collected 3-14 weeks after inoculation (Intact 1, Intact 2). Mice in the remaining three groups (GNX, CRPC 1, CRPC 2) were castrated by removing the testes. Mice were sacrificed and tumors were collected one day after castration (GNX) or 3-14 weeks after castration (CRPC 1, CRPC 2) in castration-resistant stage. 4 tumors were selected from each study group, totally 20 tumors.

2014-04-21 | E-GEOD-56829 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data