Korean J Urol.
1999 Jan;40(1):29-40.
Endocrine Therapy Inhibits Expression of Vascular Endothelial Growth Factor and Angiogenesis in Prostate Cancer
- Affiliations
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- 1Department of Urology, Dong-A University, Pusan, Korea.
- 2Department of Urology, College of Medicine, Chung-Ang University, Seoul, Korea.
Abstract
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PURPOSE: Angiogenesis is essential for the growth and metastasis of tumors. Mechanism of angiogenesis of prostate cancer remains to be defined. Vascular endothelial growth factor(VEGF) is one of the most potent angiogenic factors and we have previously demonstrated that VEGF was expressed by rat ventral prostate in an androgen dependent manner. We herein investigated whether VEGF also plays an important role in tumor angiogenesis of prostate cancer and whether endocrine therapy inhibits expression of VEGF and angiogenesis in prostate cancer. MATERIALS AND METHODS: Frozen tumor tissues were obtained from 21 patients with prostate cancer before and 3 months after endocrine therapy and angiogenic activity was analyzed by measuring microvascular density(MVD) using immunohistochemical study for factor VIII and VEGF expression by RT-PCR -Southern blot assay and immunogistochemical study, respectively. RESULTS: Prostate cancer showed significantly increased expression of VEGF and MVD as compared with normal prostatic tissues and benign hyperplastic tissues(p<0.001). There were signficant correlations between VEGF expression and MVD of prostate cancer tissues. After endocrine therapy, both MVD and VEGF expression in prostate cancer tissues were signficantly decreased as compared with those of before endocrine therapy(p<0.001). There were no signficant differences between bilateral orchiectomy and leuprolelin therapy in inihibitory effect of VEGF expression and MVD in prostate cancer tissues. CONCLUSIONS: These results suggest that VEGF may be a major angiogenic factor in prostate cancer and one of important action mechanisms of endocrine therapy in prostate cancer may be in its inhibition of VEGF expression and tumor angiogenic activity.