Stable expression of full length human androgen receptor in PC-3 prostate cancer cells enhances sensitivity to retinoic acid but not to 1?,25-dihydroxyvitamin D3

The Prostate ◽  
2003 ◽  
Vol 56 (4) ◽  
pp. 293-304 ◽  
Author(s):  
Shalini Murthy ◽  
Marco Marcelli ◽  
Nancy L. Weigel
Keyword(s):  
Prostate Cancer ◽  
Retinoic Acid ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Full Length ◽  
Stable Expression ◽  
Prostate Cancer Cells ◽  
Dihydroxyvitamin D3 ◽  
Human Androgen Receptor

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 Highly tumorigenic human androgen receptor-positive prostate cancer cells overexpress angiogenin

2007 ◽  
Vol 98 (3) ◽  
pp. 350-356 ◽  
Author(s):  
Manabu Kawada ◽  
Hiroyuki Inoue ◽  
Masayuki Arakawa ◽  
Kozo Takamoto ◽  
Tohru Masuda ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Human Androgen Receptor

scholarly journals Ralaniten Sensitizes Enzalutamide-Resistant Prostate Cancer to Ionizing Radiation in Prostate Cancer Cells that Express Androgen Receptor Splice Variants

Cancers ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1991 ◽  
Author(s):  
Carmen A. Banuelos ◽  
Yusuke Ito ◽  
Jon K. Obst ◽  
Nasrin R. Mawji ◽  
Jun Wang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Dna Damage ◽  
Androgen Receptor ◽  
Ionizing Radiation ◽  
Cancer Cells ◽  
Splice Variants ◽  
Inhibitory Effect ◽  
Full Length ◽  
Brdu Incorporation ◽  
Prostate Cancer Cells

Blocking androgen receptor (AR) transcriptional activity by androgen deprivation therapy (ADT) improves the response to radiotherapy for intermediate and high risk prostate cancer. Unfortunately, ADT, antiandrogens, and abiraterone increase expression of constitutively active splice variants of AR (AR-Vs) which regulate DNA damage repair leading to resistance to radiotherapy. Here we investigate whether blocking the transcriptional activities of full-length AR and AR-Vs with ralaniten leads to enhanced sensitivity to radiotherapy. Combination therapies using ralaniten with ionizing radiation were evaluated for effects on proliferation, colony formation, cell cycle, DNA damage, and Western blot analyses in human prostate cancer cells that express both full-length AR and AR-Vs. Ralaniten and a potent next-generation analog (EPI-7170) decreased expression of DNA repair genes whereas enzalutamide had no effect. FACS analysis revealed a dose-dependent decrease of BrdU incorporation with increased accumulation of γH2AX with a combination of ionizing radiation with ralaniten. An additive inhibitory effect on proliferation of enzalutamide-resistant cells was achieved with a combination of ralaniten compounds with ionizing radiation. Ralaniten and EPI-7170 sensitized prostate cancer cells that express full-length AR and AR-Vs to radiotherapy whereas enzalutamide had no added benefit.

609: Effects of Sirna and Phytoestrogen Treatments on the Expression of Genes Regulated through the Androgen Receptor of Lncap Prostate Cancer Cells

2004 ◽  
Vol 171 (4S) ◽  
pp. 162-162
Author(s):  
Paul Thelen ◽  
Michal Grzmil ◽  
Iris E. Eder ◽  
Barbara Spengler ◽  
Peter Burfeind ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Expression Of Genes
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