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首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >Action of fenretinide (4-HPR) on ovarian cancer and endothelial cells.
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Action of fenretinide (4-HPR) on ovarian cancer and endothelial cells.

机译：芬维A胺（4-HPR）对卵巢癌和内皮细胞的作用。

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BACKGROUND: Fenretinide (4-HPR) is a synthetic retinoid that has been reported to inhibit the growth of cancer cell lines in vitro. MATERIALS AND METHODS: We examined the effect of 4-HPR on ovarian cancer (OVCAR-5) cell proliferation, viability and invasion using standard techniques. We also examined the action of 4-HPR on the actin cytoskeleton using immunocytochemistry, and on phosphorylation of focal adhesion kinase (FAK) using immunoprecipitation and phosphotyrosine immunoblotting. We then examined the activity of 4-HPR on endothelial cells using the tube formation assay on Matrigel. RESULTS: 4-HPR inhibited OVCAR-5 cell proliferation and viability at concentrations higher than 1 microM, with 70-90% growth inhibition at 10 microM. 4-HPR (1 microM) significantly inhibited OVCAR-5 invasion after 3 days preincubation. In view of the importance of the cytoskeleton in cell motility, we examined the action of 4-HPR on the actin cytoskeleton and on FAK phosphorylation. In OVCAR-5 cells treated with 1 mM fenretinide for 3 days, actin cytoskeleton stress fibers were disrupted and FAK tyrosine phosphorylation was elevated dose-dependently. Endothelial cells treated with 1 microM 4-HPR failed to form tubes, but formed small cellular aggregates. CONCLUSION: Fenretinide has anti-tumor activity by acting on the actin cytoskeleton and by regulating FAK tyrosine phosphorylation. 4-HPR also inhibits endothelial cell tube formation, a major step in angiogenesis.
机译：背景：芬尼替尼（4-HPR）是一种合成的类维生素A，据报道可在体外抑制癌细胞系的生长。材料与方法：我们使用标准技术检查了4-HPR对卵巢癌（OVCAR-5）细胞增殖，活力和侵袭的影响。我们还使用免疫细胞化学检查了4-HPR对肌动蛋白细胞骨架的作用，并使用了免疫沉淀和磷酸酪氨酸免疫印迹法研究了粘着斑激酶（FAK）的磷酸化作用。然后，我们使用在Matrigel上进行的管形成分析检查了4-HPR对内皮细胞的活性。结果：4-HPR在高于1 microM的浓度下抑制OVCAR-5细胞的增殖和活力，在10 microM时抑制70-90％的生长。预孵育3天后，4-HPR（1 microM）显着抑制OVCAR-5入侵。考虑到细胞骨架在细胞运动中的重要性，我们检查了4-HPR对肌动蛋白细胞骨架和FAK磷酸化的作用。在用1 mM芬维A胺处理3天的OVCAR-5细胞中，肌动蛋白细胞骨架应激纤维被破坏，FAK酪氨酸磷酸化呈剂量依赖性升高。用1 microM 4-HPR处理的内皮细胞未能形成管，但形成了小的细胞聚集体。结论：芬维A胺通过作用于肌动蛋白细胞骨架并调节FAK酪氨酸磷酸化而具有抗肿瘤活性。 4-HPR还抑制内皮细胞管的形成，这是血管生成的重要步骤。

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