[Roles of highly expressed bone-specific genes in bone metastatic prostate cancer PC3 cells: Advances in studies].

Prostate cancer (PCa) is a maligmancy with high morbidity and mortality. Bone metastasis is the main cause of short survival time and difficulties in the treatment and prevention of PCa. Previous findings of our team showed 155 bone-specific genes highly expressed in bone metastatic PC3 cells, which is considered to be the key to their adaptation to the bone micro-environment, proliferation and formation of metastatic tumor, and extensively exists in cancer metastasis in multiple systems. This review summarizes the published literature on the highly expressed bone-specific genes, focusing on the roles and values of these genes in the metastasis, progression, clinical diagnosis, treatment and prognosis of PCa, offering a prospect of the direction and targets in the studies of PCa bone metastasis so as to enrich the bone metastatic theories and clinical treatment principles of this disease in the future.

[Angiogenesis and regulatory factors in rats with BPH induced by testosterone].

OBJECTIVE: To study angiogenesis and regulatory factors in the proliferated prostatic tissues of Sprague Dawley (SD) rats with BPH induced by testosterone. METHODS: Sixteen castrated SD rats, aged 8 weeks and weighing 200 approximately 250 g, were equally randomized into a model group and a control group, and the BPH model was established by subcutaneous injection of testosterone. Immunohistochemistry and MIAS (micro-image analysis system) were used to test the manifestations of MVD (microvessel density), VEGF (vascular endothelium growth factor), flk-1, endostatin, MMP-2 (matrix metalloproteinase-2) and TIMP-2 (tissue inhibitor of metalloproteinase-2) in the prostatic tissues of both the model and the control groups. Multiple linear regression with the stepwise method was adopted to analyze the data. RESULTS: The manifestations of MVD, VEGF, flk-1, MMP-2, MMP-2/TIMP-2 and VEGF/endostatin in the model group were higher, while that of endostatin was lower than in the control group (P < 0.01), and the manifestation of TIMP-2 showed no statistical difference between the two groups. The regression analysis indicated that MVD was positively correlated to VEGF, VEGF/endostatin and MMP-2/TIMP-2 (r = 0.974, 0.986, 0.982, P < 0.05) and negatively correlated to endostatin (r = - 0.975, P < 0.05) . CONCLUSION: Testosterone could induce BPH in SD rats by increasing MVD and promoting the multiplication of vascular endothelial cells after regradation of basement membrane.

[Histomorphological studies on hyperplastic prostate of castrated rat caused by androgen].

OBJECTIVES: To investigate prostatic histomorphological changes of rat benign prostatic hyperplasia (BPH) models. METHODS: After castrated, SD rats were injected subcutaneously testosterone propionate to induce the BPH. Water substitution method was used to measure prostatic volumes. Prostatic tissue were stained by hemoloxylin and eosin, the morphometric changes of glandular and interstitial tissues were semi-quantified by image analysis system. Multiple linear regression was adopted to analyze the results. RESULTS: In comparison with normal group, prostatic volumes were significantly enlarged (P < 0.01) with glands expanded and interstitial tissues increased in BPH model. Glandular average diameters, volumes and surface areas in unit volume, as well as glandular circumferences and glandular relative total volumes were all significantly increased (P < 0.01). Glandular counts, density, ratio of glandular surface area to volume. And glandular average curvature were all declined (P < 0.05-0.01), so was interstitial circumference (P < 0.01). But volume density had no changes, and relative total interstitial volumes were obviously increased. Prostatic volume was significantly correlated with glandular relative total volume (r = 0.989, P < 0.001) and interstitial relative total volume(r = 0.789, P < 0.001). Prostatic volume was also correlated significantly with glandular average volume(r = 0.789, P < 0.001). CONCLUSIONS: Action of androgen on rat prostate may mainly lie in glandular epithelial hyperplasia, which manifests enlargement of glandular lumen accompanied by hyperplasia of interstitial tissues.