scholarly journals Recruitment of NCOR1 to VDR target genes is enhanced in prostate cancer cells and associates with altered DNA methylation patterns

2012 ◽  
Vol 34 (2) ◽  
pp. 248-256 ◽  
Author(s):  
C. L. Doig ◽  
P. K. Singh ◽  
V. K. Dhiman ◽  
J. L. Thorne ◽  
S. Battaglia ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Dna Methylation ◽  
Cancer Cells ◽  
Target Genes ◽  
Prostate Cancer Cells ◽  
Methylation Patterns

Androgen receptor: acting in the three-dimensional chromatin landscape of prostate cancer cells

2011 ◽  
Vol 5 (1) ◽  
Author(s):  
Harri Makkonen ◽  
Jorma J. Palvimo
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Binding Sites ◽  
Target Genes ◽  
Three Dimensional ◽  
Regulatory Elements ◽  
Gene Promoters ◽  
Loop Formation ◽  
Prostate Cancer Cells

AbstractAndrogen receptor (AR) acts as a hormone-controlled transcription factor that conveys the messages of both natural and synthetic androgens to the level of genes and gene programs. Defective AR signaling leads to a wide array of androgen insensitivity disorders, and deregulated AR function, in particular overexpression of AR, is involved in the growth and progression of prostate cancer. Classic models of AR action view AR-binding sites as upstream regulatory elements in gene promoters or their proximity. However, recent wider genomic screens indicate that AR target genes are commonly activated through very distal chromatin-binding sites. This highlights the importance of long-range chromatin regulation of transcription by the AR, shifting the focus from the linear gene models to three-dimensional models of AR target genes and gene programs. The capability of AR to regulate promoters from long distances in the chromatin is particularly important when evaluating the role of AR in the regulation of genes in malignant prostate cells that frequently show striking genomic aberrations, especially gene fusions. Therefore, in addition to the mechanisms of DNA loop formation between the enhancer bound ARs and the transcription apparatus at the target core promoter, the mechanisms insulating distally bound ARs from promiscuously making contacts and activating other than their normal target gene promoters are critical for proper physiological regulation and thus currently under intense investigation. This review discusses the current knowledge about the AR action in the context of gene aberrations and the three-dimensional chromatin landscape of prostate cancer cells.

scholarly journals 1α,25-Dihydroxyvitamin D3 Inhibits Growth of VCaP Prostate Cancer Cells Despite Inducing the Growth-Promoting TMPRSS2:ERG Gene Fusion

Endocrinology ◽  
2010 ◽  
Vol 151 (4) ◽  
pp. 1409-1417 ◽  
Author(s):  
Michele N. Washington ◽  
Nancy L. Weigel
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Target Gene ◽  
Target Genes ◽  
Fusion Gene ◽  
Critical Factor ◽  
Synthetic Analog ◽  
Prostate Cancer Cells ◽  
Dihydroxyvitamin D3

Vitamin D receptor (VDR) agonists have been shown to reduce the growth of several prostate cancer cell lines. However, the effects of VDR activation have not been examined in the presence of the recently identified androgen-regulated TMPRSS2:ERG gene fusions, which occur in a high percentage of prostate cancers and play a role in growth and invasiveness. In a previous microarray study, we found that VDR activation induces TMPRSS2 expression in LNCaP prostate cancer cells. Here we show that the natural VDR agonist 1α,25-dihydroxyvitamin D3 and its synthetic analog EB1089 increase expression of TMPRSS2:ERG mRNA in VCaP prostate cancer cells; this results in increased ETS-related gene (ERG) protein expression and ERG activity as demonstrated by an increase in the ERG target gene CACNA1D. In VCaP cells, we were not able to prevent EB1089-mediated TMPRSS2:ERG induction with an androgen receptor antagonist, Casodex, although in LNCaP cells, as reported for some other common androgen receptor and VDR target genes, Casodex reduces EB1089-mediated induction of TMPRSS2. However, despite inducing the fusion gene, VDR agonists reduce VCaP cell growth and expression of the ERG target gene c-Myc, a critical factor in VDR-mediated growth inhibition. Thus, the beneficial effects of VDR agonist treatment override some of the negative effects of ERG induction, although others remain to be tested.

scholarly journals GSTP1 DNA Methylation and Expression Status Is Indicative of 5-aza-2′-Deoxycytidine Efficacy in Human Prostate Cancer Cells

PLoS ONE ◽  
2011 ◽  
Vol 6 (9) ◽  
pp. e25634 ◽  
Author(s):  
Karen Chiam ◽  
Margaret M. Centenera ◽  
Lisa M. Butler ◽  
Wayne D. Tilley ◽  
Tina Bianco-Miotto
Keyword(s):  
Prostate Cancer ◽  
Dna Methylation ◽  
Cancer Cells ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Expression Status

scholarly journals Cyclin-dependent kinase 5 acts as a critical determinant of AKT-dependent proliferation and regulates differential gene expression by the androgen receptor in prostate cancer cells

2015 ◽  
Vol 26 (11) ◽  
pp. 1971-1984 ◽  
Author(s):  
Julia Lindqvist ◽  
Susumu Y. Imanishi ◽  
Elin Torvaldson ◽  
Marjo Malinen ◽  
Mika Remes ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Target Genes ◽  
Growth Promotion ◽  
Intracellular Localization ◽  
Prostate Cancer Cells ◽  
Promoting Effect ◽  
Akt Activation

Contrary to cell cycle–associated cyclin-dependent kinases, CDK5 is best known for its regulation of signaling processes in differentiated cells and its destructive activation in Alzheimer's disease. Recently, CDK5 has been implicated in a number of different cancers, but how it is able to stimulate cancer-related signaling pathways remains enigmatic. Our goal was to study the cancer-promoting mechanisms of CDK5 in prostate cancer. We observed that CDK5 is necessary for proliferation of several prostate cancer cell lines. Correspondingly, there was considerable growth promotion when CDK5 was overexpressed. When examining the reasons for the altered proliferation effects, we observed that CDK5 phosphorylates S308 on the androgen receptor (AR), resulting in its stabilization and differential expression of AR target genes including several growth-priming transcription factors. However, the amplified cell growth was found to be separated from AR signaling, further corroborated by CDK5-depdent proliferation of AR null cells. Instead, we found that the key growth-promoting effect was due to specific CDK5-mediated AKT activation. Down-regulation of CDK5 repressed AKT phosphorylation by altering its intracellular localization, immediately followed by prominent cell cycle inhibition. Taken together, these results suggest that CDK5 acts as a crucial signaling hub in prostate cancer cells by controlling androgen responses through AR, maintaining and accelerating cell proliferation through AKT activation, and releasing cell cycle breaks.

scholarly journals Selenite reactivates silenced genes by modifying DNA methylation and histones in prostate cancer cells

2008 ◽  
Vol 29 (11) ◽  
pp. 2175-2181 ◽  
Author(s):  
Nong Xiang ◽  
Rui Zhao ◽  
Guoqing Song ◽  
Weixiong Zhong
Keyword(s):  
Prostate Cancer ◽  
Dna Methylation ◽  
Cancer Cells ◽  
Prostate Cancer Cells

scholarly journals Triptolide Inhibits Histone Methyltransferase EZH2 and Modulates the Expression of Its Target Genes in Prostate Cancer Cells

2013 ◽  
Vol 14 (10) ◽  
pp. 5663-5669 ◽  
Author(s):  
Ousman Tamgue ◽  
Cheng-Sen Chai ◽  
Lin Hao ◽  
John-Clotaire Daguia Zambe ◽  
Wei-Wei Huang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Target Genes ◽  
Histone Methyltransferase ◽  
Prostate Cancer Cells

scholarly journals DNA methylation changes following DNA damage in prostate cancer cells

Epigenetics ◽  
2019 ◽  
Vol 14 (10) ◽  
pp. 989-1002 ◽  
Author(s):  
Laura P. Sutton ◽  
Sarah A. Jeffreys ◽  
Jessica L. Phillips ◽  
Phillippa C. Taberlay ◽  
Adele F. Holloway ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Dna Methylation ◽  
Dna Damage ◽  
Cancer Cells ◽  
Prostate Cancer Cells

scholarly journals Switch to full-length of XAF1 mRNA expression in prostate cancer cells by the DNA methylation inhibitor

2006 ◽  
Vol 118 (10) ◽  
pp. 2485-2489 ◽  
Author(s):  
Xiaolei Fang ◽  
Zhaoxu Liu ◽  
Yidong Fan ◽  
Chengyun Zheng ◽  
Sten Nilson ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Dna Methylation ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Full Length ◽  
Prostate Cancer Cells ◽  
Methylation Inhibitor ◽  
Dna Methylation Inhibitor
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