Siomycin A treatment in prostate cancer cell lines PC3 and LNCaP
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE36531 | GEO | 2012/10/19
SECONDARY ACCESSION(S): PRJNA153401
REPOSITORIES: GEO
Similar Datasets
Project description:Siomycin A treatment in prostate cancer cell lines resulted in a concurrent inhibition of specific cell cycle genes and strongly impaired cell viability. Illumina microarray experiments were done using PC3 and LNCaP cell lines treated with 0.5 microM Siomaycin A either 24h or 48h in triplicates.
2012-10-19 | E-GEOD-36531 | biostudies-arrayexpress
Project description:The bone metastasis-derived PC3 and the lymph node metastasis-derived LNCaP prostate cancer cell lines are widely studied, having been described in thousands of publications over the last four decades. Here, we report short-read whole-genome sequencing (WGS) and de novo assembly of PC3 (ATCC CRL-1435) and LNCaP (clone FGC; ATCC CRL-1740) at ?70 × coverage. A known homozygous mutation in TP53 and homozygous loss of PTEN were robustly identified in the PC3 cell line, whereas the LNCaP cell line exhibited a larger number of putative inactivating somatic point and indel mutations (and in particular a loss of stop codon events). This study also provides preliminary evidence that loss of one or both copies of the tumor suppressor Capicua (CIC) contributes to primary tumor relapse and metastatic progression, potentially offering a treatment target for castration-resistant prostate cancer (CRPC). Our work provides a resource for genetic, genomic, and biological studies employing two commonly-used prostate cancer cell lines.
| S-EPMC5473753 | biostudies-literature
Project description:Study aimed at evaluating differences in Du145, PC3 and LNCaP human prostate cancer cells treated with ATX-101 and docetaxel for 24h.
2017-12-31 | E-MTAB-4858 | biostudies-arrayexpress
Project description:MiRNAs are small non-coding RNAs that regulate the expression of specific mRNA targets mainly by translational repression, mRNA deadenylation or cleavage. This series is meant to identify miRNAs deregulated in prostate cancer (PCa) by comparing the PCa cell lines LNCaP, PC3 and Du-145 to the normal prostate epithelial cell line RWPE-1.
2012-03-08 | GSE17317 | GEO
Project description:MiRNAs are small non-coding RNAs that regulate the expression of specific mRNA targets mainly by translational repression, mRNA deadenylation or cleavage. This series is meant to identify miRNAs deregulated in prostate cancer (PCa) by comparing the PCa cell lines LNCaP, PC3 and Du-145 to the normal prostate epithelial cell line RWPE-1. We analyzed three arrays each for LNCaP, PC3, Du-145 and RWPE-1 cell lines
2012-03-08 | E-GEOD-17317 | biostudies-arrayexpress
Project description:LSD1 (also known as KDM1A) is a histone demethylase and a key regulator of gene expression in embryonic stem cells and cancer.1,2 LSD1 was initially identified as a transcriptional repressor via its demethylation of active histone H3 marks (di-methyl lysine 4 [2MK4]).1 In prostate cancer, specifically, LSD1 also co-localizes with the AR and demethylates repressive 2MK9 histone marks from androgen-responsive AR target genes, facilitating androgen-mediated induction of AR-regulated gene expression and androgen-induced proliferation in androgen-dependent cancers.3,4 Recently, it was shown that treatment with high doses of androgens (e.g.10-fold higher doses than those required for induction of expression of androgen-activated genes such as PSA) recruits LSD1 and AR to an enhancer within the AR; this AR and LSD1 recruitment represses AR transcription.5 Thus, LSD1 appears to play a role in mediating both the proliferative and repressive phases of the biphasic androgen dose-response curve. For these reasons, we hypothesized that LSD1 might be important for maintenance of AR signaling in castration-resistant prostate cancer (CRPC) tumors. However, in this report, we describe a distinct role of LSD1 as a driver of proliferation and survival of prostate cancer cells, including CRPC cells, irrespective of androgens or even AR expression. Specifically, LSD1 activates expression of cell cycle, mitosis, and embryonic stem cell maintenance pathways that are enriched in lethal prostate cancers – pathways not activated by androgens. Finally, we observe that treatment with a new LSD1 inhibitor potently and specifically suppresses LSD1 function and suppresses CRPC growth and survival in vitro and in vivo. Our data place LSD1 as a key driver of androgen-independent survival in lethal prostate cancers and demonstrate the potential of LSD1-directed therapies in the near-term. 1. Shi Y, Lan F, Matson C, et al. Histone demethylation mediated by the nuclear amine oxidase homolog LSD1. Cell. Dec 29 2004;119(7):941-953. 2. Whyte WA, Bilodeau S, Orlando DA, et al. Enhancer decommissioning by LSD1 during embryonic stem cell differentiation. Nature. Feb 9 2012;482(7384):221-225. 3. Metzger E, Wissmann M, Yin N, et al. LSD1 demethylates repressive histone marks to promote androgen-receptor-dependent transcription. Nature. Sep 15 2005;437(7057):436-439. 4. Yamane K, Toumazou C, Tsukada Y, et al. JHDM2A, a JmjC-containing H3K9 demethylase, facilitates transcription activation by androgen receptor. Cell. May 5 2006;125(3):483-495. 5. Cai C, He HH, Chen S, et al. Androgen receptor gene expression in prostate cancer is directly suppressed by the androgen receptor through recruitment of lysine-specific demethylase 1. Cancer Cell. Oct 18 2011;20(4):457-471.
2018-12-31 | GSE59009 | GEO
Project description:Human prostate cancer cell lines treated with androgen receptor (AR) agonists/antagonists and concurrent glucocorticoid receptor (GR) agonist/antagonists
2017-08-18 | GSE97204 | GEO
Project description:Comparison of miRNA expression profiles directly comparing PC3 cells to LNCaP cells using unamplified and amplified miRNA. Keywords: Expression profiling of hormone sensitive vs. insensitive prostate cancer cell lines and evaluation of amplification fidelity
2006-04-05 | GSE4572 | GEO
Project description:BACKGROUND: Malignancy alters cellular complex lipid metabolism and membrane lipid composition and turnover. Here, we investigated whether tumorigenesis in cancer-derived prostate epithelial cell lines influences protein kinase C-linked turnover of ethanolamine phosphoglycerides (EtnPGs) and alters the pattern of ethanolamine (Etn) metabolites released to the medium. METHODS: Prostate epithelial cell lines P4E6, LNCaP and PC3 were models of prostate cancer (PCa). PNT2C2 and PNT1A were models of benign prostate epithelia. Cellular EtnPGs were labelled with [1-(3)H]-Etn hydrochloride. PKC was activated with phorbol ester (TPA) and inhibited with Ro31-8220 and GF109203X. D609 was used to inhibit PLD (phospholipase D). [(3)H]-labelled Etn metabolites were resolved by ion-exchange chromatography. Sodium oleate and mastoparan were tested as activators of PLD2. Phospholipase D activity was measured by a transphosphatidylation reaction. Cells were treated with ionomycin to raise intracellular Ca(2+) levels. RESULTS: Unstimulated cell lines release mainly Etn and glycerylphosphorylEtn (GPEtn) to the medium. Phorbol ester treatment over 3h increased Etn metabolite release from the metastatic PC3 cell line and the benign cell lines PNT2C2 and PNT1A but not from the tumour-derived cell lines P4E6 and LNCaP; this effect was blocked by Ro31-8220 and GF109203X as well as by D609, which inhibited PLD in a transphosphatidylation reaction. Only metastatic PC3 cells specifically upregulated Etn release in response to TPA treatment. Oleate and mastoparan increased GPEtn release from all cell lines at the expense of Etn. Ionomycin stimulated GPEtn release from benign PNT2C2 cells but not from cancer-derived cell lines P4E6 or PC3. Ethanolamine did not stimulate the proliferation of LNCaP or PC3 cell lines but decreased the uptake of choline (Cho). CONCLUSIONS: Only the metastatic basal PC3 cell line specifically increased the release of Etn on TPA treatment most probably by PKC activation of PLD1 and increased turnover of EtnPGs. The phosphatidic acid formed will maintain a cancer phenotype through the regulation of mTOR. Ethanolamine released from cells may reduce Cho uptake, regulating the membrane PtdEtn:PtdCho ratio and influencing the action of PtdEtn-binding proteins such as RKIP and the anti-apoptotic hPEBP4. The work highlights a difference between LNCaP cells used as a model of androgen-dependent early stage PCa and androgen-independent PC3 cells used to model later refractory stage disease.
| S-EPMC4200097 | biostudies-other
Project description:We measured the effect of docetaxel treatment to three differentially responsive prostate cancer cell lines, LNCaP, DU145 and PC-3, based on a transcriptional time course response by microarray analysis. These cell lines represent both androgen independent (DU145 and PC-3) and androgen sensitive (LNCaP) cells
2016-07-21 | GSE83654 | GEO