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穿心莲内酯通过抑制 FLT3 信号、脂肪酸合成和细胞铁摄取来抑制 MV4-11 细胞增殖。

Andrographolide Suppresses MV4-11 Cell Proliferation through the Inhibition of FLT3 Signaling, Fatty Acid Synthesis and Cellular Iron Uptake.

机构信息

The State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing 210023, China.

Department of Oncology, Clinical Research Institute, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou 310014, China.

出版信息

Molecules. 2017 Aug 31;22(9):1444. doi: 10.3390/molecules22091444.

DOI:10.3390/molecules22091444
PMID:28858244
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6151431/
Abstract

: Andrographolide (ADR), the main active component of , displays anticancer activity in various cancer cell lines, among which leukemia cell lines exhibit the highest sensitivity to ADR. In particular, ADR was also reported to have reduced drug resistance in multidrug resistant cell lines. However, the mechanism of action (MOA) of ADR's anticancer and anti-drug-resistance activities remain elusive. : In this study, we used the MV4-11 cell line, a FLT3 positive acute myeloid leukemia (AML) cell line that displays multidrug resistance, as our experimental system. We first evaluated the effect of ADR on MV4-11 cell proliferation. Then, a quantitative proteomics approach was applied to identify differentially expressed proteins in ADR-treated MV4-11 cells. Finally, cellular processes and signal pathways affected by ADR in MV4-11 cell were predicted with proteomic analysis and validated with in vitro assays. : ADR inhibits MV4-11 cell proliferation in a dose- and time-dependent manner. With a proteomic approach, we discovered that ADR inhibited fatty acid synthesis, cellular iron uptake and FLT3 signaling pathway in MV4-11 cells. : ADR inhibits MV4-11 cell proliferation through inhibition of fatty acid synthesis, iron uptake and protein synthesis. Furthermore, ADR reduces drug resistance by blocking FLT3 signaling.

摘要

: 穿心莲内酯（ADR）是 的主要活性成分，在各种癌细胞系中显示出抗癌活性，其中白血病细胞系对 ADR 的敏感性最高。特别是，ADR 还被报道在多药耐药细胞系中降低了耐药性。然而，ADR 的抗癌和抗耐药活性的作用机制（MOA）仍然难以捉摸。: 在这项研究中，我们使用 MV4-11 细胞系作为实验系统，该细胞系是一种 FLT3 阳性急性髓系白血病（AML）细胞系，表现出多药耐药性。我们首先评估了 ADR 对 MV4-11 细胞增殖的影响。然后，应用定量蛋白质组学方法鉴定 ADR 处理的 MV4-11 细胞中差异表达的蛋白质。最后，通过蛋白质组学分析预测 ADR 对 MV4-11 细胞中受影响的细胞过程和信号通路，并通过体外实验进行验证。: ADR 以剂量和时间依赖的方式抑制 MV4-11 细胞增殖。通过蛋白质组学方法，我们发现 ADR 抑制了 MV4-11 细胞中的脂肪酸合成、细胞内铁摄取和 FLT3 信号通路。: ADR 通过抑制脂肪酸合成、铁摄取和蛋白质合成来抑制 MV4-11 细胞增殖。此外，ADR 通过阻断 FLT3 信号通路降低了耐药性。

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