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首页> 外文期刊>Journal of Cellular Physiology >Suppression of interactions between prostate tumor cell-surface integrin and endothelial ICAM-1 by simvastatin inhibits micrometastasis
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Suppression of interactions between prostate tumor cell-surface integrin and endothelial ICAM-1 by simvastatin inhibits micrometastasis

机译：抑制前列腺肿瘤之间的相互作用细胞表面整合素和内皮ICAM-1辛伐他汀抑制微小转移

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摘要

Cancer micrometastasis relies on the ability of cancer cells to secrete angiogenic modulators, to interact with the vascular endothelium, and to overcome the resistance offered by the endothelial-barrier. Being an essential step prior to metastasis, blockage of micrometastasis can have potential applications in cancer therapy and metastasis prevention. Due to poorly known molecular mechanisms leading to micrometastasis, developing therapeutic strategies to target prostate cancer utilizing drugs that block micrometastasis is far from reality. Here, we demonstrate the potential benefits of simvastatin in the inhibition of prostate cancer micrometastasis and reveal the novel molecular mechanisms underlying this process. First, we showed that simvastatin inhibited the ability of human PC3 prostate cancer cells for transendothelial migration in vitro. Second, our data indicated that simvastatin modulates the expression of tumor-derived factors such as angiopoietins and VEGF-A at the mRNA and protein levels by the PC3 cells, thus preventing endothelial-barrier disruption. Third, simvastatin directly activated endothelial cells and enhances endothelial-barrier resistance. Apart from this, our study revealed that simvastatin-mediated effect on PC3 micrometastasis was mediated through inhibition of integrin αvβ3 activity and suppression of interaction between prostate cancer cell integrin αvβ3 with endothelial ICAM-1.
机译：癌症微小转移依赖的能力肿瘤细胞分泌血管生成调节器,与血管内皮,克服提供的阻力endothelial-barrier。在转移之前,微小转移的堵塞有潜在的应用在癌症治疗吗预防和转移。分子机制导致微小转移,发展中治疗策略目标利用药物阻止前列腺癌微小转移远离现实。演示辛伐他汀的潜在好处在前列腺癌的抑制微小转移,小说揭示了分子机制这一过程。表明辛伐他汀抑制的能力人类生物前列腺癌细胞transendothelial迁移体外。数据表明,辛伐他汀调节表达tumor-derived等因素组和VEGF-A信使rna和蛋白质水平的生物细胞,从而防止endothelial-barrier破坏。辛伐他汀直接激活内皮细胞并提高endothelial-barrier阻力。除此之外,我们的研究显示,simvastatin-mediated对生物的影响微小转移是通过抑制介导的v的整合素αβ3活性和抑制前列腺癌的细胞整合素之间的相互作用α与内皮ICAM-1 vβ3。

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