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首页> 外文期刊>BMC Complementary and Alternative Medicine >Total saponins of Bolbostemma paniculatum (maxim.) Franquet exert antitumor activity against MDA-MB-231 human breast cancer cells via inhibiting PI3K/Akt/mTOR pathway
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Total saponins of Bolbostemma paniculatum (maxim.) Franquet exert antitumor activity against MDA-MB-231 human breast cancer cells via inhibiting PI3K/Akt/mTOR pathway

机译:Bolbostemma Paniculatum(Maxim。)果仁植物的总皂苷通过抑制PI3K / AKT / MTOR途径对MDA-MB-231人乳腺癌细胞产生抗肿瘤活性

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BACKGROUND:The aim of the present study was to examine the effects of the Bolbostemma paniculatum (Maxim.) Franquet (BP) active compound, BP total saponins (BPTS), on MDA-MB-231 cells, and investigate the underlying mechanism regarding BPTS-mediated attenuation of the PI3K/Akt/mTOR pathway.METHODS:The effect of BPTS on cytotoxicity, induction of apoptosis and migration on MDA-MB-231 cells at three different concentrations was investigated. A CCK-8 assay, wound-healing assay and flow cytometry were used to demonstrate the effects of BPTS. Additionally, expression of the primary members of the PI3K/Akt/mTOR signaling pathway was assessed using western blotting. To verify the underlying mechanisms, a PI3K inhibitor and an mTOR inhibitor were used.RESULTS:BPTS inhibited proliferation of MDA-MB-231 cells with an IC50 value of 10?μg/mL at 48?h. BPTS inhibited migration of MDA-MB-231 cells, and the western blot results demonstrated that BPTS reduced p-PI3K, p-Akt and p-mTOR protein expression levels in MDA-MB-231 cells. Additionally, the results were confirmed using a PI3K inhibitor and an mTOR inhibitor. BPTS decreased proliferation and migration of MDA-MB-231 cells possibly through inhibiting the PI3K/Akt/mTOR signaling pathway.CONCLUSIONS:The results highlight the therapeutic potential of BPTS for treating patients with triple-negative breast cancer.
机译:背景:本研究的目的是检测血栓血症胰腺炎(MAXIM。)Franquet(BP)活性化合物,BP总皂苷(BPT),MDA-MB-231细胞的影响,并研究了关于BPT的潜在机制研究了PI3K / AKT / MTOR途径的衰减。研究了BPTS对三种不同浓度下的MDA-MB-231细胞对细胞毒性,诱导凋亡和迁移的影响。 CCK-8测定,伤口愈合测定和流式细胞术用于证明BPT的作用。另外,使用蛋白质印迹评估PI3K / AKT / MTOR信号传导途径的主要成员的表达。为了验证潜在的机制,使用PI3K抑制剂和MTOR抑制剂。结果:BPTS在48℃下抑制MDA-MB-231细胞的增殖,IC50值为10≤μg/ ml。 BPT抑制MDA-MB-231细胞的迁移,Western印迹结果表明,在MDA-MB-231细胞中,BPT减少了P-PI3K,P-AKT和P-MTOR蛋白表达水平。另外,使用PI3K抑制剂和MTOR抑制剂证实结果。 BPTS可能通过抑制PI3K / AKT / MTOR信号传导途径来降低MDA-MB-231细胞的增殖和迁移。结论:结果突出了BPT治疗三重阴性乳腺癌患者的治疗潜力。

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