ABSTRACT
<p><b>OBJECTIVE</b>To establish an implanted model of human colonic carcinoma on chick embryo, and to study the effects of anti-angiopoietin-2 antibody on its vascularization.</p><p><b>METHODS</b>The human colonic adenocarcinoma cell line HT-29 was transplanted on the chick embryo's chorioallantoic membrane(CAM), and the angiogenesis characteristics were observed by stero-microscope, light microscope and immunohistochemistry. Furthermore, the effects of anti-angiopoietin-2 antibody on angiogenesis and tumor growth were also investigated.</p><p><b>RESULTS</b>Three to seven days after HT-29 cell line was implanted into CAM, tumors grew rapidly and new blood vessels grew toward tumors. Five days after anti-angiopoietin-2 antibody was given, the number of blood vessels in anti-angiopoietin-2 antibody group was significantly down-regulated than that in tumor control group observed by stero-microscope (37.2+/-4.6 vs 56.8+/-7.4, P<0.01), but was up-regulated than that in normal control group (37.2+/-4.6 vs 9.6+/-2.4, P<0.01). Microvessel density(MVD) in anti-angiopoietin-2 antibody group was much lower than that in tumor control group by histological examination (9.6+/-2.4 vs 20.2+/-5.8, P<0.01).</p><p><b>CONCLUSION</b>Angiopoietin-2 antibody is able to inhibit the angiogenesis induced by colorectal cancer cell line HT-29 obviously. The anti-angiopoietin-2 antibody may be potentially useful for clinical treatment of colonic carcinoma.</p>
Subject(s)
Animals , Chick Embryo , Humans , Angiopoietin-2 , Allergy and Immunology , Antibodies, Monoclonal , Pharmacology , Colonic Neoplasms , HT29 Cells , Neoplasm Transplantation , Neovascularization, PathologicABSTRACT
Objective To study the expression and the relation of vascular endothelial growth factor (VEGF)and matrix metal proteinase-2(MMP-2)in rectal cancer and evaluate their roles in rectal carcinogen- esis and development.Methods The expression of VEGF and MMP-2 in 52 cases of rectal cancer was de- tected by immunohistochemical SP technique.12 cases normal rectal tissue served as the control group.Re- suits The expression of VEGF in rectal carcinoma(67.3 %)was much higher than that in control group(P
ABSTRACT
<p><b>OBJECTIVE</b>To study the role of the basic fibroblast growth factor (bFGF) and transforming growth factor beta1 (TGF-beta1) in benign prostatic hyperplasia (BPH).</p><p><b>METHODS</b>The human stromal cells of BPH were isolated and cultured. The proliferation of the stromal cells cultured in serum-free medium was detected by MTT method, the phenotype changes of smooth muscle cells detected by immunohistochemical method, and the effect of different concentrations of bFGF and TGF-beta1 on the cultured stromal cells of BPH observed.</p><p><b>RESULTS</b>bFGF stimulated the cultured BPH stromal cell proliferation (P < 0.05, P < 0.01) and decreased the expression of smooth muscle cell (SMC) phenotype in higher concentration (10 microg/L). TGF-beta1 (> 1 microg/L) inhibited stromal cell proliferation and increased the expression of SMC phenotype (P < 0.05, P < 0.01). 5 microg/ml bFGF and TGF-beta1 (0.001 microg/L, 0.01 microg/L) promoted stromal cell proliferation (P < 0.01), while 5 microg/L bFGF and TGF-beta1 (0.1 microg/L, 1 microg/L, 10 microg/L) inhibited it, slightly in 0.1 microg/L (P > 0.05) and significantly in 1 microg/L and 10 microg/L (P < 0.01), and increased the expression of SMC phenotype in higher concentration (> 1 microg/L, P < 0.01).</p><p><b>CONCLUSION</b>bFGF stimulates the proliferation of the prostatic stromal cells of BPH in a time- and dose-dependent fashion and decreases the expression of SMC phenotype, TGF-beta1 inhibits the growth of stromal cells and induces the differentiation of stromal cells to SMC, both playing an important role in the mechanism of BPH.</p>