Background :Triple-negative breast cancer (TNBC) is a subtype of invasive cancer in breast with the symptoms of unfavourable prognosis and limited targeted treatment options. Evidence of changes in the metabolic status of TNBC, characterised by increased glycolysis, mitochondrial oxidative phosphorylation, as well as production and utilization of tricarboxylic acid cycle intermediates.Objective:Investigate the proteins altered in cryptotanshinone treated MDA-MB-231 cells and explore the key pathways and specific molecular markers involved in cryptotanshinone treatment.Method:We use unlabeled quantitative proteomics to gain insight into the anticancer mechanism of cryptotanshinone on MDA-MB231 triple negative breast cancer cells. And flow cytometry was used to detect apoptosis and changes in cell mitochondrial membrane potential.Results:We show that inhibiting the expression of electron transport chain complex proteins, also inhibits mitochondrial oxidative phosphorylation. Additionally, down-regulation of the ribosime biogenesis pathway was found to inhibit cell metabolism. Conclusion:In summary, results show that cryptotanshinone can trigger rapid and irreversible apoptosis in MDA-MB-231 cells through effectively inhibiting cell metabolism.

中文翻译：

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隐丹参酮对 MDA-MB231 细胞线粒体代谢的有效抑制：蛋白质组学分析

背景：三阴性乳腺癌（TNBC）是乳腺浸润性癌症的一种亚型，具有预后不良和靶向治疗选择有限的症状。TNBC 代谢状态变化的证据，其特征是糖酵解增加、线粒体氧化磷酸化以及三羧酸循环中间体的产生和利用。目的：研究隐丹参酮处理的 MDA-MB-231 细胞中蛋白质的改变并探索关键隐丹参酮治疗中涉及的途径和特定分子标志物。方法：我们使用未标记的定量蛋白质组学来深入了解隐丹参酮对 MDA-MB231 三阴性乳腺癌细胞的抗癌机制。并采用流式细胞仪检测细胞凋亡和细胞线粒体膜电位的变化。结果：我们表明，抑制电子传递链复合蛋白的表达，也会抑制线粒体氧化磷酸化。此外，发现核糖体生物合成途径的下调会抑制细胞代谢。结论：综上所述，结果表明隐丹参酮可通过有效抑制细胞代谢引发MDA-MB-231细胞快速且不可逆的凋亡。