Similar Datasets
Project description:We report the application of ChIP and RNA sequencing to identify the mechanism whereby stable overexpression of MED19 in androgen-dependent LNCaP cells promotes growth under conditions of androgen deprivation. We determined the MED19 and AR transcriptomes and cistromes in control and MED19 LNCaP cells. We also examined genome-wide H3K27 acetylation in both the absence and presence of androgens. We found that MED19 overexpression selectively alters AR occupancy, H3K27 acetylation, and gene expression. Under conditions of androgen deprivation, genes regulated by MED19 correspond to genes regulated by ELK1, a transcription factor that binds the AR N-terminus to induce select AR target gene expression and proliferation. This study provides important insight into the mechanisms of prostate cancer cell growth under low androgen, and underscores the importance of the MED19 in this process.
2021-01-20 | GSE161170 | GEO
Project description:We report the application of ChIP and RNA sequencing to identify the mechanism whereby stable overexpression of MED19 in androgen-dependent LNCaP cells promotes growth under conditions of androgen deprivation. We determined the MED19 and AR transcriptomes and cistromes in control and MED19 LNCaP cells. We also examined genome-wide H3K27 acetylation in both the absence and presence of androgens. We found that MED19 overexpression selectively alters AR occupancy, H3K27 acetylation, and gene expression. Under conditions of androgen deprivation, genes regulated by MED19 correspond to genes regulated by ELK1, a transcription factor that binds the AR N-terminus to induce select AR target gene expression and proliferation. This study provides important insight into the mechanisms of prostate cancer cell growth under low androgen, and underscores the importance of the MED19 in this process.
2021-01-20 | GSE161167 | GEO
Project description:Prostate cancer is the most common cancer in men and cardiac glycosides inhibit prostate cancer cell proliferation. In order to investigate the mechanism by which cardiac glycosides inhibit prostate cancer cells, we observed genome-wide RNA expression in prostate cancer LNCaP-abl cells, hormone resistant cells, after the cardiac glycoside treatment using RNA-Seq. In addition, we profiled LNCaP-abl cells after androgen receptor (AR) knockdown to observe whether cardiac glycoside effect on RNA expression is similar to that of AR knockdown. Observation of three cardioglycosides, Digoxin, Peruvoside and Strophanthidin, and AR knockdown regulated RNA expression in LNCaP-abl with RNA-Seq (each triplicates)
2012-04-03 | E-GEOD-35126 | biostudies-arrayexpress
Project description:FoxA1 has been shown critical for prostate development and prostate-specific gene expression regulation. In addition to its well-established role as an AR pioneering factor,several studies have recently revealed significant AR binding events in prostate cancer cells with FoxA1 knockdown. Furthermore, the role of FoxA1 itself in prostate cancer has not been carefully examined. Thus, it is important to understand the role of FoxA1 in prostate cancer and how it interacts with AR signaling. To address these questions, we generated LNCaP cells with stable FoxA1 knockdown. We performed AR/FoxA1 ChIP-seq and microarray analysis of these cells. ChIP_Seq examination of AR and FoxA1 binding sites in LNCaP shCtrl and shFoxA1 cells
2014-06-02 | E-GEOD-37345 | biostudies-arrayexpress
Project description:We used RNA-Seq to profile gene expression in LNCaP cells with and without PRMT1 knockdown.
2022-01-28 | GSE195659 | GEO
Project description:Prostate cancer is the most common cancer in men and cardiac glycosides inhibit prostate cancer cell proliferation. In order to investigate the mechanism by which cardiac glycosides inhibit prostate cancer cells, we observed genome-wide RNA expression in prostate cancer LNCaP-abl cells, hormone resistant cells, after the cardiac glycoside treatment using RNA-Seq. In addition, we profiled LNCaP-abl cells after androgen receptor (AR) knockdown to observe whether cardiac glycoside effect on RNA expression is similar to that of AR knockdown.
2012-04-04 | GSE35126 | GEO
Project description:Genome wide expression changes following 50uM Casodex treatment were investigated to determine regulatory targets commonly overlooked in gene function specific microarrays and for comparison of the effects of the mutant androgen receptor (AR) LNCaP cell line against the wild-type AR expressing PC-346C cells. LNCaP Prostate Cancer cells were treated for a period of 48h with or without 50uM Casodex following a 24h seeding period. At the selected time point, total RNA was harvested from the cells for hybridization and analysis by Nimblgen Systems Inc using the homo sapiens gene expression array.
2007-09-15 | E-GEOD-8533 | biostudies-arrayexpress
Project description:FoxA1 has been shown critical for prostate development and prostate-specific gene expression regulation. In addition to its well-established role as an AR pioneering factor,several studies have recently revealed significant AR binding events in prostate cancer cells with FoxA1 knockdown. Furthermore, the role of FoxA1 itself in prostate cancer has not been carefully examined. Thus, it is important to understand the role of FoxA1 in prostate cancer and how it interacts with AR signaling. To address these questions, we generated LNCaP cells with stable FoxA1 knockdown. We performed AR/FoxA1 ChIP-seq and microarray analysis of these cells.
2014-06-02 | GSE37345 | GEO
Project description:Genome wide expression changes following 50uM Casodex treatment were investigated to determine regulatory targets commonly overlooked in gene function specific microarrays and for comparison of the effects of the mutant androgen receptor (AR) LNCaP cell line against the wild-type AR expressing PC-346C cells. Keywords: Expression response to treatment, will be used with another array dataset for cell type comparison.
2007-09-15 | GSE8533 | GEO
Project description:Elevated levels of androgen receptor (AR) in prostate cancer confer resistance to current antiandrogens and play a causal role in disease progression due to persistent target gene activation. Through pharmacologic and genetic approaches, we show that half of all direct AR target genes, including TMPRSS2, the primary driver of ETS fusion transcripts in 70 percent of human prostate cancers, require histone deacetylase (HDAC) activity for transcriptional activation by AR. Surprisingly, the HDAC3-NCoR complex, which typically functions to repress gene expression by nuclear receptors, is required for AR target gene activation. Prostate cancer cells treated with HDAC inhibitors have reduced AR protein levels, but we show that the mechanism of blockade of AR activity is through failure to assemble a coactivator/RNA polymerase II complex after AR binds to the enhancers of target genes. Failed complex assembly is associated with a phase shift in the cyclical wave of AR recruitment that typically occurs in response to ligand treatment. HDAC inhibitors retain the ability to block AR activity in hormone refractory prostate cancer models and therefore merit clinical investigation in this setting. HDAC-regulated AR target genes defined here can serve as biomarkers to ensure sufficient levels of HDAC inhibition. Experiment Overall Design: LNCaP prostate cancer cells were grown in charcoal stripped, androgen deplete medium. They were then stimulated with or without 1nM R1881 and with or without two doses of HDAC inhibitors TSA, SAHA, and LBH 589. Cyclohexamide was include to block new protein synthesis. Cells were harvested 16 hours after treatment.
2009-01-09 | E-GEOD-9000 | biostudies-arrayexpress