Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA114795 | ENA |
REPOSITORIES: ENA
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Project description:Time series of the prostate cancer cell line LNCaP, treated for 2, 4, 6 and 8 hours with the synthetic androgen R1881. As control, the cells were cultured for 2, 4, 6 and 8 hours in the presence of the same concentration of solvent (ethanol). With this short treatment time, we aimed to identify mainly direct targets of the androgen receptor. LNCaP has a very low growth rate in steroid stripped medium and resumes growth on addition of androgens. Keywords: Time course
2006-04-01 | GSE4027 | GEO
Project description:The catalytic subunit of the human telomerase (hTERT) is activated during tumorigenesis in many cancers including prostate cancer (PCa). Androgens mediate their effect through the androgen receptor (AR), a key factor controlling PCa growth. hTERT expression is known to be regulated by androgens, however contrarily observed to be inhibited or activated. Here, we reveal that androgens repress or activate hTERT expression in a concentration-dependent manner. Low physiological androgen levels activate while supraphysiological androgen levels (SAL) repress hTERT expression. We confirmed SAL-mediated gene repression of hTERT in native human PCa samples derived from patients treated ex vivo as well as in cancer spheroids derived from androgen-dependent and castration resistant PCa (CRPC) cells. Interestingly, based on chromatin immunoprecipitation (ChIP) data both a positive androgen response element (pARE) at -4kb distal and a negative response element (nARE) at the proximal -0.1kb promoter region were identified. Focusing on the nARE it was narrowed down to -121 to -58 bp in the core promoter region. ChIP experiments confirmed an androgen-dependent recruitment of AR and the tumor suppressors inhibitor of growth 1 and 2 (ING1 and ING2), recently identified as AR co-repressors. Mechanistically, the knockdown of either ING1 or ING2 reduced androgen-mediated repression of hTERT indicating that ING1 and ING2 mediate AR-regulated transrepression on the hTERT expression. Thus, our data suggest a dual, biphasic function of AR to control hTERT expression by transactivation and transrepression. The inhibition of hTERT by androgens by a nARE located in the proximal promoter region is mediated at least in part by the AR co-repressors ING1 and ING2.
2022-03-04 | GSE155528 | GEO
Project description:Androgen receptor RIP-seq of LNCaP cells treated with androgen hormone
| PRJNA392760 | ENA
Project description:Aberrant androgen receptor (AR)-mediated transcription is a critical driver in progression of human prostate cancer. It's known that different doses of androgens can elicit differential transcriptional and proliferative responses in prostate-tumor cells. Here, we set out to examine the androgenic regulation of glycoprotein expression in the membrane fraction of prostate-tumor cells that could serve as mediators or markers of androgen-induced proliferative responses observed in prostate-tumor cells. A bioanalytical workflow involving lectin-affinity chromatography and label-free quantitative mass spectrometry was used to identify androgen-sensitive glycomembrane protein expression associated with androgen-mediated proliferation. This study would facilitate the identification of surface membrane proteins involved in androgen-mediated proliferation and provide potential therapeutic targets in the detection treatment of proliferation prostate-tumors.
2022-03-01 | PXD002913 | Pride
Project description:We compared PC3 cells with or without harboring the wild-AR construct in the growth conditions of 1nM R1881, 10nM R1881 and ethanol (the solvent for R1881). The MOCK control is PC3 cells transfected with the empty vectors. Experiment Overall Design: 2 PC3 Samples transfected with empty vector, without R1881, 2 PC3 Samples transfected with AR, treated with Ethanol, 2 PC3 Samples transfected with AR, treated with 1nM R1881, 1 PC3 transfected with AR, treated with 10nM R1881.
2009-03-15 | E-GEOD-15091 | biostudies-arrayexpress
Project description:Transcription profiling by array of human amnion epithelial FL cells treated with the carcinogen BPDE at low concentration
2025-01-16 | E-GEOD-10979 | ExpressionAtlas
Project description:Prostate epithelial cells depend on androgens for survival and function. In early prostate cancer, besides survival, androgens also regulated tumor growth, which is exploited by androgen ablation/ blockade therapies in metastatic disease. The aim of the present study was to characterize the role of the androgen receptor pathway in prostate cancer progression and to identify potential disease markers. Microarray analysis was used to establish the androgen-regulated gene expression profile, upon stimulation with the synthetic androgen R1881 or the antiandrogen hydroxyflutamide, of the androgen-responsive PC346C cell line and its derivative castration-resistant sublines: PC346DCC (vestigial AR levels), PC346Flu1 (AR overexpression) and PC346Flu2 (T877A mutated AR)
2011-08-05 | GSE22914 | GEO
Project description:Background: Aldo-keto reductase (AKR) 1C family member 3 (AKR1C3), one of four identified human AKR enzymes, catalyzes steroid, prostaglandin, and xenobiotic metabolism. In the prostate, AKR1C3 is up-regulated in localized and advanced prostate adenocarcinoma, and is associated with prostate cancer (PCa) aggressiveness. Here we provide initial evidence for potential roles of AKR1C3 in PCa progression. Methods: Spatial distribution of AKR1C3 was analyzed using immunohistochemical staining in prostate adenocarcinoma tissue array. Human PCa PC-3 cells were stably transfected with AKR1C3 cDNA to establish PC3-AKR1C3 transfectants. Microarray and bioinformatics analyses were performed to identify pathways that are activated by elevated AKR1C3 expression in PCa cells. Functional confirmation of microarray and bioinformatics results was performed by immunoblot analysis and an in vitro Matrigel angiogenesis assay. Results: Elevated AKR1C3 expression was specifically limited to human prostate adenocarcinoma. Microarray and bioinformatics analysis suggested that elevated AKR1C3 expression in PC-3 cells modulates estradiol and androgen metabolism and activates insulin growth factor (IGF)-1 and Akt signaling pathways. Immunoblots confirmed that phosphorylated levels of IGF-1 receptor (IGF-1R) and Akt are significantly up-regulated in PC3-AKR1C3 as compared to mock transfectants. PC3-AKR1C3 transfectants promoted endothelial cell tube formation in Matrigel as compared to parental PC-3 cells and mock transfectants. Conclusion: Microarray and bioinformatics data followed by biological analyses suggest that elevated AKR1C3 expression in PC-3 cells promotes PCa angiogenesis and aggressiveness. These results suggest AKR1C3 can promote the aggressiveness of PCa through modulating estrogen and androgen metabolism with subsequent activation of growth factor IGF-1 and cytoplasmic Akt signaling pathways. Total RNA from mock- and ACR1C3 transfected PC-3 cells was isolated, with 2 or 3 biological replicates each. Gene expression data from AKR1C3 transfected PC-3 cells were compared with mock-transfected data.
2010-08-10 | E-GEOD-20956 | biostudies-arrayexpress
Project description:Genome wide DNA methylation profiling of androgen-sensitive and –refractory prostate cancer cells. The Illumina Infinium HumanMethylation450 Beadchip was used to obtain DNA methylation profiles across approximately 480.000 CpGs in Prostate cancer cell lines showing different sensitivity to hormonal treatments. Samples included the androgen receptor negative cell lines PC3 and DU145, the androgen sensitive cell line LNCaP and the LNCaP abl cell line expressing androgen receptor but refractory prostate cancer cell line to hormonal treatments.
2023-12-31 | GSE217962 | GEO