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首页> 外文期刊>Nutrition and Cancer: An International Journal >Procyanidins from evening primrose (Oenothera paradoxa) Defatted seeds inhibit invasiveness of breast cancer cells and modulate the expression of selected genes involved in angiogenesis, metastasis, and apoptosis
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Procyanidins from evening primrose (Oenothera paradoxa) Defatted seeds inhibit invasiveness of breast cancer cells and modulate the expression of selected genes involved in angiogenesis, metastasis, and apoptosis

机译:来自傍晚报春花(Oenothera Paradoxa)脱差的种子的原因抑制乳腺癌细胞的侵袭性,并调节参与血管生成,转移和细胞凋亡的所选基因的表达

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摘要

There is a growing interest in plant polyphenols (including flavanols) that exhibit pleiotropic biological activities such as antiinflammatory, antioxidant, and anticancer effects. Here, we report for the first time the inhibition of MDA-MB-231 breast cancer cell viability and invasiveness by an evening primrose flavanol preparation (EPFP). We observed a decrease in MDA-MB-231 viability of 50% vs. a control after 72 h of incubation with EPFP at a concentration of 58 μM gallic acid equivalents (GAE) and an inhibition of their invasiveness of 65% vs. a control at 75 μM GAE after 48 h of incubation. EPFP caused a 10-fold reduction in matrix metalloproteinase-9 (MMP-9) activity at 100 μM GAE. Furthermore, through modulation of mRNA expression, EPFP reduced the expression levels of the following proteins: antiapoptotic Bcl-2, angiogenic vascular endothelial growth factor (VEGF), and 2 transcription factors (c-Jun, c-Fos). Moreover, analysis by flow cytometry revealed that EPFP induced apoptosis in MDA-MB-231 cells. In conclusion, our data shows that EPFP inhibits cell viability by increasing apoptosis and decreases cell invasiveness by decreasing angiogenesis.
机译:植物多酚(包括黄烷醇)的兴趣日益增长,表现出抗炎,抗氧化剂和抗癌效果如抗炎生物活性。在这里,我们首次报告MDA-MB-231乳腺癌细胞活力和侵袭性的夜晚报春花黄烷醇制剂(EPFP)。我们观察到50%Vs的MDA-MB-231活力降低。与EPFP的浓度为58μm,无食酸当量(GAE)的孵育和抑制它们的侵袭性65%与对照的抑制剂在孵育48小时后,在75μmgae。 EPFP在100μmgae下引起基质金属蛋白酶-9(MMP-9)活性的10倍。此外,通过调节mRNA表达,EPFP降低了以下蛋白质的表达水平:抗透露Bcl-2,血管生成血管内皮生长因子(VEGF)和2种转录因子(C-JUN,C-FOS)。此外,流式细胞仪的分析显示EPFP诱导MDA-MB-231细胞的细胞凋亡。总之,我们的数据表明,EPFP通过增加细胞凋亡并通过降低血管生成来降低细胞侵袭性来抑制细胞活力。

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    Department of Medical Enzymology Medical University of Lodz Mazowiecka 6/8 92-215 Lodz Poland;

    Department of Medical Enzymology Medical University of Lodz Mazowiecka 6/8 92-215 Lodz Poland;

    Department of Medical Enzymology Medical University of Lodz Mazowiecka 6/8 92-215 Lodz Poland;

    Department of Medical Enzymology Medical University of Lodz Mazowiecka 6/8 92-215 Lodz Poland;

    Institute of Technical Biochemistry Technical University of Lodz Lodz Poland;

    Institute of Technical Biochemistry Technical University of Lodz Lodz Poland;

    Department of Medical Enzymology Medical University of Lodz Mazowiecka 6/8 92-215 Lodz Poland;

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  • 正文语种 eng
  • 中图分类 肿瘤学;
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