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首页> 外文期刊>Nutrition and Cancer: An International Journal >Breast Cancer Cell Apoptosis is Synergistically Induced by Curcumin, Trastuzumab, and Glutathione Peroxidase-1 but Robustly Inhibited by Glial Cell Line-Derived Neurotrophic Factor
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Breast Cancer Cell Apoptosis is Synergistically Induced by Curcumin, Trastuzumab, and Glutathione Peroxidase-1 but Robustly Inhibited by Glial Cell Line-Derived Neurotrophic Factor

机译:通过姜黄素,曲妥珠单抗和谷胱甘肽过氧化物酶-1,但通过胶质细胞系衍生的神经营养因子协同诱导乳腺癌细胞凋亡

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ABSTRACT We hypothesized that synergy between curcumin (CURC), trastuzumab (TZMB), and glutathione peroxidase-1 (GPX-1) accelerates breast cancer (BC) cell apoptosis which is inhibited by glial cell line-derived neurotrophic factor (GDNF). We measured survival of BC cell lines treated or cotreated with CURC and TZMB, and then with GDNF, before measuring expression levels of growth and apoptosis genes, These experiments were also repeated on SKBR3 cells transiently expressing GPX-1. CURC+TZMB cotreatment induced BC cell apoptosis more significantly than single treatment. GDNF highly inhibited CURC+TZMB toxicity and restored survival. Ectopic overexpression of GPX-1 per se induced SKBR3 cell death that was accelerated upon CURC+TZMB cotreatment. This substantial death induction was inhibited by GDNF more robustly than in single-treated cells. All these changes correlated with changes in expression levels of key molecules and were further confirmed by flow cytometry and correlation analysis.
机译:摘要我们假设姜黄素(CURC),曲妥珠单抗(TZMB)和谷胱甘肽过氧化物酶-1(GPX-1)之间的协同作用加速了通过胶质细胞系衍生的神经营养因子(GDNF)抑制的乳腺癌(BC)细胞凋亡。我们测量了用莪术和TZMB处理或分配的BC细胞系的存活,然后用GDNF在测量生长和凋亡基因的表达水平之前,在短暂表达GPX-1的SKBR3细胞上还重复这些实验。 Curc + TZMB Cotreatment诱导BC细胞凋亡比单次处理更显着。 GDNF高度抑制杂志+ TZMB毒性并恢复存活。 GPX-1本身的异位过度表达诱导的SKBR3细胞死亡,其在Curc + TZMB CoTreatment上加速。这种大量死亡诱导受到GDNF比在单处理细胞中更强烈的诱导。所有这些改变与关键分子表达水平的变化相关,并通过流式细胞术和相关分析进一步证实。

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