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Triterpenoid Saponin AG8 from Ardisia gigantifolia stapf. Induces Triple Negative Breast Cancer Cells Apoptosis through Oxidative Stress Pathway

机译:Triterpenoid Saponin Ag8来自Ardisia Gigantifolia Stapf。通过氧化应激途径诱导三重阴性乳腺癌细胞凋亡

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摘要

Triple-negative breast cancers (TNBCs) are associated with poor patient survival because of the absence of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) expressions. Our previous studies have shown that the triterpenoid saponin AG8 from Ardisia gigantifolia stapf. inhibits the proliferation of MDA-MB-231 cells. In this study, the effects of AG8 were further analyzed in different TNBC cell types: MDA-MB-231, BT-549, and MDA-MB-157 cells. AG8 inhibited the viability of MDA-MB-231, BT-549, and MDA-MB-157 cells in a dose-dependent manner and showed stronger cytotoxicity to African American (AA) and mesenchymal (M) subtypes than Caucasian (CA) and mesenchymal stem-like (MSL) subtypes, respectively. AG8 impaired the uptake of MitoTracker Red CMXRos by the mitochondria of TNBC cells in a dose-dependent manner, and this was recovered by N-acetyl-L-cysteine (NAC). AG8 affected GSH, SOD, and MDA levels of TNBC cells, but different TNBC subtypes had different sensitivities to AG8 and NAC. In addition, we found that AG8 increased the Bax/Bcl-2 ratio and the levels of cytoplasmic cytochrome c and significantly decreased phosphorylation of ERK and AKT in BT549 and MDA-MB-157 cells. AG8 elicited its anticancer effects through ROS generation, ERK and AKT activation, and by triggering mitochondrial apoptotic pathways in TNBC cells. AG8 had selective cytotoxic effects against the AA and M TNBC subtypes and markedly induced MDA-MB-157 (AA subtype) cell apoptosis through pathways that were not associated with ROS, which was different from the other two subtypes. The underlying mechanisms should be further investigated.
机译:三阴性乳腺癌(TNBCs)与患者存活差,因为不存在雌激素受体(ER),孕酮受体(PR)和人表皮生长因子受体2(HER2)的表达式相关联。我们以前的研究表明,从虎gigantifolia麻黄的三萜皂甙AG8。抑制MDA-MB-231细胞的增殖。在这项研究中,进一步分析在不同TNBC细胞类型AG8的效果:MDA-MB-231,BT-549和MDA-MB-157细胞。 AG8抑制MDA-MB-231,BT-549,和生存能力MDA-MB-157细胞以剂量依赖的方式和显示更强的细胞毒性非裔美国人(AA)和间充质(M)亚型比高加索人(CA)和间充质干状(MSL)亚型,分别。 AG8受损的MitoTracker红CMXRos的摄取TNBC细胞以剂量依赖的方式线粒体,和这是由N-乙酰基-L-半胱氨酸(NAC)回收。 AG8影响TNBC细胞的GSH,SOD和MDA水平,但不同亚型TNBC有不同的敏感性,AG8和NAC。此外,我们发现,AG8增加了Bax蛋白/ Bcl-2的比率和胞质细胞色素c的水平和显著在BT549和MDA-MB-157细胞减少ERK和AKT的磷酸化。 AG8引起通过ROS产生,ERK和AKT活化其抗癌作用,并通过在TNBC细胞触发线粒体凋亡通路。 AG8具有针对通过通路未用ROS相关联的AA和M TNBC亚型和显着诱导的MDA-MB-157(AA亚型)细胞凋亡,这是与其他两个亚型的不同选择性的细胞毒性效应。基本的机制应进一步调查。

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