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首页> 外文期刊>Molecular and Cellular Biology >Peroxisome Proliferator-Activated Receptor γ Regulates E-Cadherin Expression and Inhibits Growth and Invasion of Prostate Cancer
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Peroxisome Proliferator-Activated Receptor γ Regulates E-Cadherin Expression and Inhibits Growth and Invasion of Prostate Cancer

机译：过氧化物酶体增殖物激活的受体γ调节E-钙黏着蛋白表达并抑制前列腺癌的生长和侵袭。

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Peroxisome proliferator-activated receptor γ (PPARγ) might not be permissive to ligand activation in prostate cancer cells. Association of PPARγ with repressing factors or posttranslational modifications in PPARγ protein could explain the lack of effect of PPARγ ligands in a recent randomized clinical trial. Using cells and prostate cancer xenograft mouse models, we demonstrate in this study that a combination treatment using the PPARγ agonist pioglitazone and the histone deacetylase inhibitor valproic acid is more efficient at inhibiting prostate tumor growth than each individual therapy. We show that the combination treatment impairs the bone-invasive potential of prostate cancer cells in mice. In addition, we demonstrate that expression of E-cadherin, a protein involved in the control of cell migration and invasion, is highly up-regulated in the presence of valproic acid and pioglitazone. We show that E-cadherin expression responds only to the combination treatment and not to single PPARγ agonists, defining a new class of PPARγ target genes. These results open up new therapeutic perspectives in the treatment of prostate cancer.
机译：过氧化物酶体增殖物激活受体γ（PPARγ）可能不允许前列腺癌细胞中的配体激活。在最近的一项随机临床试验中，PPARγ与抑制因子或PPARγ蛋白的翻译后修饰的关联可能解释了PPARγ配体缺乏作用。使用细胞和前列腺癌异种移植小鼠模型，我们在这项研究中证明，使用PPARγ激动剂吡格列酮和组蛋白脱乙酰基酶抑制剂丙戊酸的联合治疗比每种单独的疗法在抑制前列腺肿瘤生长方面更有效。我们表明联合治疗损害小鼠前列腺癌细胞的骨侵袭潜力。另外，我们证明在丙戊酸和吡格列酮存在下，E-钙粘着蛋白（一种参与细胞迁移和侵袭控制的蛋白）的表达高度上调。我们显示，E-钙粘着蛋白表达仅对组合治疗有反应，对单个PPARγ激动剂无反应，从而定义了新型的PPARγ靶基因。这些结果为前列腺癌的治疗开辟了新的治疗前景。

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