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Home > References > 2013 > Suppression of DHT-induced paracrine stimulation of endothelial cell growth by estrogens via prostate cancer cells.

Suppression of DHT-induced paracrine stimulation of endothelial cell growth by estrogens via prostate cancer cells.

Wen J, Zhao Y, Li J, Weng C, Cai J, Yang K, Yuan H, Imperato-McGinley J, Zhu YS.
Journal   Prostate
Species  
Analytes Measured   Flt-1 VEGFR1
Matrix Tested   Cell culture supernatants
Year   2013
Volume  
Page Numbers  
Application   Angiogenesis and Vascular
Abstract
BACKGROUND: Androgen modulation of angiogenesis in prostate cancer may be not directly mediated by androgen receptor (AR) as AR is not detected in the prostatic endothelial cells.

METHODS: We examined the paracrine stimulation of cell proliferation by prostate tumor cells and its modulation by androgen and estrogens in a murine endothelial cell line (MEC) that does not express AR.

RESULTS: Tumor cell conditioned media (TCM) collected from LAPC-4 or LNCaP prostatic tumor cells produced a time- and concentration-dependent induction of cell growth in MECs, which was parallel to the VEGF concentration in the TCM. This TCM-induced cell growth in MECs was enhanced by the treatment of prostatic tumor cells with dihydrotestosterone (DHT). Both the TCM-stimulation and DHT-enhancement effects in MECs were completely blocked by SU5416, a specific VEGF receptor antagonist. Co-administration of 17α-estradiol or 17β-estradiol with DHT in prostatic tumor cells completely inhibited the DHT-enhancement effect while treatment with DHT, 17α-estradiol or 17β-estradiol did not produce any significant direct effect in MECs. Moreover, administration of 17α-estradiol or 17β-estradiol in xenograft animals with LAPC-4 or LNCaP prostate tumor significantly decreased the microvessel number in the tumor tissues.

CONCLUSIONS: Our study indicated that prostate tumor cells regulate endothelial cell growth through a paracrine mechanism, which is mainly mediated by VEGF; and DHT is able to modulate endothelial cell growth via tumor cells, which is inhibited by 17α-estradiol and 17β-estradiol. Thus, both17α-estradiol and 17β-estradiol are potential agents for anti-angiogenesis therapy in androgen-responsive prostate cancer.

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