Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA341958 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4174981.fastq.gz | Fastqsanger.gz | |||
| SRR4174982.fastq.gz | Fastqsanger.gz | |||
| SRR4174983.fastq.gz | Fastqsanger.gz | |||
| SRR4174985.fastq.gz | Fastqsanger.gz | |||
| SRR4174987.fastq.gz | Fastqsanger.gz |
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Project description:Androgens are required for both normal prostate development and prostate carcinogenesis. We used DNA microarrays, representing approximately 18,000 genes, to examine the temporal program of gene expression following treatment of the human prostate cancer cell line LNCaP with a synthetic androgen. We observed statistically significant changes in levels of transcripts of more than 500 genes. Many of these genes were previously reported androgen targets, but most were not previously known to be regulated by androgens. The androgen-induced expression programs in 3 additional androgen-responsive human prostate cancer cell lines, and in 4 androgen-independent subclones derived from LNCaP, shared many features with those observed in LNCaP, but some differences were observed. A remarkable fraction of the genes induced by androgen appeared to be related to production of seminal fluid and these genes included many that play roles in protein folding, trafficking, and secretion. Prostate cancer cell lines retain features of androgen responsiveness that reflect normal prostatic physiology. These results provide a broad view of the effect of androgen signaling on the transcriptional program in these cancer cells, and a foundation for further studies of androgen action Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Computed
2005-10-15 | E-GEOD-3451 | biostudies-arrayexpress
Project description:Androgens are required for both normal prostate development and prostate carcinogenesis. We used DNA microarrays, representing approximately 18,000 genes, to examine the temporal program of gene expression following treatment of the human prostate cancer cell line LNCaP with a synthetic androgen. We observed statistically significant changes in levels of transcripts of more than 500 genes. Many of these genes were previously reported androgen targets, but most were not previously known to be regulated by androgens. The androgen-induced expression programs in 3 additional androgen-responsive human prostate cancer cell lines, and in 4 androgen-independent subclones derived from LNCaP, shared many features with those observed in LNCaP, but some differences were observed. A remarkable fraction of the genes induced by androgen appeared to be related to production of seminal fluid and these genes included many that play roles in protein folding, trafficking, and secretion. Prostate cancer cell lines retain features of androgen responsiveness that reflect normal prostatic physiology. These results provide a broad view of the effect of androgen signaling on the transcriptional program in these cancer cells, and a foundation for further studies of androgen action Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set
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Project description:Although androgen deprivation therapy triggers a rapid response in men with metastatic prostate cancer, most patients eventually progress to lethal castration resistant prostate cancer (CRPC) characterized by androgen receptor (AR)-dependent tumor growth despite castrate levels of circulating androgens. Current treatment options for CRPC remain limited and non-curative, rendering improved outcomes dependent on deeper mechanistic insight and new therapeutic targets. In this RNA sequencing study we profiled the transcriptomes of SPOP WT and mutant LNCaP cells before and after androgen deprivation by RNA-sequencing. Using standard criteria (minimum 2-fold change), we identified 981 genes that were differentially expressed in SPOP mutant vs SPOP WT LNCaP cells grown in the absence of androgens . Strikingly, a significant fraction (595 or ~60%) of these genes overlapped with genes (3510 in number) differentially expressed as a function of androgen in WT LNCaP cells, indicating partial restoration of AR signaling in SPOP mutant cells following androgen withdrawal. To determine the contribution of GLI3 to this process, we performed RNA-sequencing following GLI3 knockdown in androgen-deprived SPOP mutant LNCaP cells. Among the 595 androgen-responsive genes in LNCaP cells whose hormone-independent expression is regulated by SPOP 187 (or ~31%) are also regulated by GLI3, thus revealing a prominent role for GLI3 in restoration of AR signaling in SPOP mutant cells following androgen withdrawal. Enrichment analysis using Gene Ontology Biological Processes revealed these 187 GLI3-regulated genes to be prominently linked with “chromosome segregation”, “DNA replication”, “transcriptional regulation of in G1/S transition”, “regulation of mitotic cell cycle”, and “chromatin silencing” among others, suggesting possible molecular genetic bases for androgen independent growth of SPOP mutant cells. Taken together, these findings indicate that SPOP mutant prostate cancer cells acquire robust androgen-independent growth through reestablishment of an AR signaling axis that involves functional crosstalk with the SHH/GLI3 pathway.
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Project description:Male sex predispose to many kidney diseases. Considering that androgens exert deleterious effects in a variety of cell types within kidney, we hypothesized that dihydrotestosterone (DHT) would impair the biology of the renal tubular cell by inducing changes in the proteome. We employed stable isotope labeling with amino acids (SILAC) in an indirect spike-in fashion to accurately quantify the proteome in DHT- and 17β-estradiol (EST)-treated human proximal tubular epithelial cells (PTEC), in 4 different experiments. Of the 5043 quantified proteins, 76 were differentially regulated. Biological processes related to energy metabolism were significantly enriched among DHT-regulated proteins. SILAC ratios of 3 candidates representing glycolysis, N-acetylglucosamine metabolism and fatty acid β-oxidation, namely glucose-6-phosphate isomerase (GPI), glucosamine-6-phosphate-N-acetyltransferase 1 (GNPNAT1) and mitochondrial trifunctional protein subunit alpha (HADHA), were verified in vitro. In vivo, renal GPI and HADHA protein expression was increased in males. Furthermore, male sex was associated to higher GPI, GNPNAT1 and HADHA protein expression in diabetic Akita mice. Functional group enrichment analysis revealed a link between our DHT-regulated proteins and glycosphingolipid metabolism within the male kidney. This is the most in depth quantitative proteomic study of human primary PTEC response to sex hormone treatment. In this study we open new perspectives on how to explore the molecular mechanisms responsible for the deleterious effects of androgens in the context of kidney disease, especially diabetic nephropathy.
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