| 秦亮,陈安民,郭风劲,等.罗格列酮对前列腺癌细胞血管生成拟态的影响.骨科,2015,6(6): 285-289. |
| 罗格列酮对前列腺癌细胞血管生成拟态的影响 |
| Effect of rosiglitazone on vasculogenic mimicry in prostate cancer cell line PC-3 |
| 投稿时间：2015-07-21 |
| DOI：10.3969/j.issn.1674-8573.2015.06.002 |
| 中文关键词: 前列腺肿瘤 过氧化物酶体增殖物激活受体 罗格列酮 血管生成拟态 |
| 英文关键词: Prostatic neoplasms Peroxisome proliferator-activated receptors Rosiglitazone Vasculogenic mimicry |
| 基金项目:教育部新教师基金项目（200804871051）；湖北省卫生厅青年人才基金（QJX2010-5） |
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| 中文摘要: |
| 目的 探讨过氧化物酶体增殖物激活受体γ（peroxisome proliferator-activated receptor γ，PPARγ）配体罗格列酮（rosiglitazone，RGZ）对前列腺癌PC-3细胞血管生成拟态的影响。方法 体外培养人前列腺癌PC-3细胞，应用细胞增殖与毒性检测（Cell Counting Kit-8，CCK-8）法观察罗格列酮不同浓度和不同作用时间对前列腺癌PC-3细胞增殖的影响；体外建立matrigel三维培养系统，观察罗格列酮对PC-3细胞血管生成拟态（vasculogenic mimicry，VM） 形成的影响；应用RT-qPCR和ELISA的方法检测血管内皮钙黏蛋白（vascular endothelial cadherin，VE-cadherin）、EphA2、血管内皮生长因子（vascular endothelial growth factor，VEGF）mRNA和 VEGF蛋白的表达。结果 罗格列酮在48 h后明显抑制前列腺癌PC-3细胞增殖,且呈时间和剂量依赖性。前列腺癌PC-3细胞在体外三维培养条件下能够形成环状和网络样结构。罗格列酮能够抑制PC-3细胞VEGF、VE-cadherin、EphA2 mRNA及VEGF蛋白的表达，并使其形成血管生成拟态的能力明显降低。结论 罗格列酮可能通过下调前列腺癌细胞VEGF、VE-cadherin、EphA2的表达抑制血管生成拟态形成。 |
| 英文摘要: |
| Objective To investigate the effect of rosiglitazone （RGZ）, the ligand of peroxisome proliferator-activated receptor γ （PPARγ）, on vasculogenic mimicry in human prostate cancer cell line PC-3 in vitro and to reveal the related molecular mechanisms. Methods PC-3 cells were cultured in vitro. The effect of RGZ with different concentrations （0.1, 1.0 and 10.0 μmol/L） and different action durations （1 to 6 days） on the growth of PC-3 cells was detected by Cell Counting Kit-8 （CCK-8） assay. A 3-dimensional cell culture system for PC-3 cells was established to observe vasculogenic mimicry formation. The change of vasculogenic mimicry formation under RGZ treatment was observed. Realtime-quantitative polymerase chain reaction （RT-qPCR） was used to detect the effect of RGZ on the mRNA expression of VEGF, VE-cadherin, and EphA2, respectively. The expression of VEGF protein was analyzed by ELISA. Results RGZ significantly inhibited the cell proliferation after 48 h in a dose- and time-dependent manner. PC-3 cells could form patterned matrix VM or tubular VM in 3-demintional culture system. RGZ markedly reduced VM density or formed shorter tubular VM in 0.1, 1.0, 10.0 μmol/L groups than in control group. After treatment with RGZ for 48 h, the expression levels of VEGF, VE-cadherin, and EphA2 mRNA were decreased in RST-treated group as compared with control group. Meantime, RGZ inhibited VEGF protein secretion, respectively. Conclusion The results indicated that activation of PPARγ by RGZ can inhibit VM formation in PC-3 cells, which may be through down-regulation of the expression of VEGF, VE-cadherin and EphA2. |
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