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首页> 外文期刊>Journal of biochemical and molecular toxicology >Fisetin induces apoptosis in breast cancer MDA‐MB‐453 cells through degradation of HER2/neu and via the PI3K/Akt pathway
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Fisetin induces apoptosis in breast cancer MDA‐MB‐453 cells through degradation of HER2/neu and via the PI3K/Akt pathway

机译:通过HER2 / NEU和PI3K / AKT途径诱导乳腺癌MDA-453细胞中的细胞凋亡诱导乳腺癌MDA-MB-453细胞凋亡

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Abstract Overexpression of human epidermal growth factor receptor 2 (HER2) is observed in breast cancer. The major snag?faced by the human population is the development of chemoresistance to HER2 inhibitors by advanced stage breast cancer cells. Moreover, recent researchers focussed on fisetin as an antiproliferative and chemotherapeutic agent. Therefore, this study was intended to analyze the effects of fisetin on HER2/neu‐overexpressing breast cancer cell lines. Our results depicted that fisetin induced apoptosis of these cells by various mechanisms, such as inactivation of the receptor, induction of proteasomal degradation, decreasing its half‐life, decreasing enolase phosphorylation, and alteration of phosphatidylinositol 3‐kinase/Akt signaling.
机译:摘要在乳腺癌中观察到人表皮生长因子受体2(HER2)的过度表达。 主要的障碍是面对人口的是通过晚期乳腺癌细胞对HER2抑制剂的化学抑制剂的发展。 此外,最近的研究人员侧重于Fisetin作为抗增殖和化学治疗剂。 因此,该研究旨在分析Fisetin对HER2 / Neu过表达乳腺癌细胞系的影响。 我们的结果表明,Fisetin通过各种机制诱导这些细胞的细胞凋亡,例如受体的灭活,诱导蛋白酶体降解,降低其半衰期,降低烯醇酶磷酸化,以及磷脂酰肌醇3-激酶/ AKT信号传导的改变。

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