scholarly journals Inhibition of tumor growth and sensitization to chemotherapy by RNA interference targeting interleukin-6 in the androgen-independent human prostate cancer PC3 model

2011 ◽  
Vol 102 (4) ◽  
pp. 769-775 ◽  
Author(s):  
Iori Sakai ◽  
Hideaki Miyake ◽  
Tomoaki Terakawa ◽  
Masato Fujisawa
Keyword(s):  
Prostate Cancer ◽  
Rna Interference ◽  
Tumor Growth ◽  
Interleukin 6 ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Inhibition Of Tumor Growth ◽  
Androgen Independent

A new mechanism of estrogen action in prostate cancer: Inhibition of tissue androgen production and prostate cancer growth by Estradiol in androgen independent prostate cancer xenografts

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 15509-15509
Author(s):  
B. Montgomery ◽  
P. Nelson ◽  
D. L. Hess ◽  
R. Vessella ◽  
E. Corey
Keyword(s):  
Prostate Cancer ◽  
Estrogen Receptor ◽  
Tumor Growth ◽  
Receptor Antagonist ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Ici 182,780 ◽  
Estrogen Receptor Antagonist ◽  
Serum Androgens ◽  
Androgen Independent

15509 Background: Estrogens are effective agents in treating prostate cancer in patients in which serum androgens are already at ‘castrate‘ or anorchid levels. The mechanisms whereby estrogens inhibit ‘androgen-independent‘ prostate cancer are unclear. Methods: The androgen-independent human prostate cancer xenograft LuCaP 35V was implanted into orchiectomized male SCID mice and established tumors were treated with placebo pellets, 17β-estradiol (E2) slow-release pellets or E2 with the estrogen receptor antagonist ICI 182,780 as previously described (Clin Cancer Res 8:1003). Effects of E2 on tumor growth and tissue testosterone (T) and dihydrotestosterone (DHT) levels were evaluated by radioimmunoassay. Results: E2 significantly inhibited growth of androgen-independent LuCaP35V ( ∼35% inhibition at 4 weeks, p=0.0047, and increased survival of tumor bearing animals, (p trend =0.03) . The estrogen receptor antagonist ICI 182,780 did not block E2 inhibition of tumor growth, suggesting a receptor independent mechanism of tumor suppression. We then examined the effect of E2 on tissue T and DHT. E2 suppressed levels of tumor T and DHT in treated tumors. Tissue androgens in placebo treated LuCaP35V xenografts were; T=1.21 (± 0.18) pg/mg and DHT=3.54 (±1.07) pg/mg, and in E2-treated LuCaP35V T=0.23 (±0.09) pg/mg and DHT =0.44 (±0.14) pg/mg, (p<0.001). Levels of T and DHT in control liver tissue from both placebo and E2-treated animals were equivalent, at less than 0.2 pg/mg. Conclusions: We have shown that E2 inhibits growth of the androgen- independent human prostate cancer xenograft LuCaP35V, and that this inhibition is estrogen receptor independent. E2 significantly suppressed tumor tissue T and DHT suggesting a new mechanism of E2 mediated growth inhibition of androgen independent prostate cancer, potentially through inhibition of tumoral steroidogenesis. This model of ‘intracrine‘ tumor androgen production can be used to evaluate other inhibitors of tissue steroidogenesis. No significant financial relationships to disclose.

Establishment and characterization of androgen-independent human prostate cancer cell lines, PcBra1, PcBra2, and PcBra3

2009 ◽  
Vol 46 (2) ◽  
pp. 123-130
Author(s):  
Camila B. Piantino ◽  
Juliana M. Sousa-Canavez ◽  
Marta Bellodi-Privato ◽  
Miguel Srougi ◽  
Luiz Heraldo Camara-Lopes ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Human Prostate Cancer Cell ◽  
Prostate Cancer Cell Lines ◽  
Androgen Independent
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