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下调哺乳动物雷帕霉素靶蛋白(mTOR)通路介导丹皮酚-铂(II)复合物在人甲状腺癌细胞和小鼠 SW1736 肿瘤异种移植中的作用。

Down-Regulation of the Mammalian Target of Rapamycin (mTOR) Pathway Mediates the Effects of the Paeonol-Platinum(II) Complex in Human Thyroid Carcinoma Cells and Mouse SW1736 Tumor Xenografts.

机构信息

Department of General Surgery, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China (mainland).

出版信息

Med Sci Monit. 2020 Jun 28;26:e922561. doi: 10.12659/MSM.922561.

Abstract

BACKGROUND This study aimed to investigate the effects of the paeonol-platinum(II) (PL-Pt[II]) complex on SW1736 human anaplastic thyroid carcinoma cell line and the BHP7-13 human thyroid papillary carcinoma cell line in vitro and on mouse SW1736 tumor xenografts in vivo. MATERIAL AND METHODS The cytotoxic effects of the PL-Pt(II) complex on SW1736 cells and BHP7-13 cells was measured using the MTT assay. Western blot measured the expression levels of cyclins, cell apoptotic proteins, and signaling proteins. DNA content and apoptosis were detected by flow cytometry. SW1736 cell thyroid tumor xenografts were established in mice followed by treatment with the PL-Pt(II) complex. RESULTS Treatment of the SW1736 and BHP7-13 cells with the PL-Pt(II) complex reduced cell proliferation in a dose-dependent manner, with an IC50 of 1.25 µM and 1.0 µM, respectively, and increased the cell fraction in G0/G1phase, inhibited p53, cyclin D1, promoted p27 and p21 expression, and significantly increased the sub-G1 fraction. Treatment with the PL-Pt(II) complex increased caspase-3 degradation, reduced the expression of p-4EBP1, p-4E-BP1 and p-S6, and reduced the expression of p-ERK1/2 and p-AKT. Treatment with the PL-Pt(II) complex reduced the volume of the SW1736 mouse tumor xenografts on day 14 and day 21, and reduced AKT phosphorylation and S6 protein expression and increased degradation of caspase-3. CONCLUSIONS The cytotoxic effects of the PL-Pt(II) complex in human thyroid carcinoma cells, including activation of apoptosis and an increased sub-G1 cell fraction of the cell cycle, were mediated by down-regulation of the mTOR pathway.

摘要

背景

本研究旨在探讨丹皮酚-铂(II)(PL-Pt[II])复合物对 SW1736 人甲状腺未分化癌细胞系和 BHP7-13 人甲状腺乳头状癌细胞系的体外作用以及对小鼠 SW1736 肿瘤异种移植物的体内作用。

材料和方法

采用 MTT 法测定 PL-Pt(II) 复合物对 SW1736 细胞和 BHP7-13 细胞的细胞毒性作用。Western blot 检测细胞周期蛋白、细胞凋亡蛋白和信号转导蛋白的表达水平。通过流式细胞术检测 DNA 含量和细胞凋亡。建立 SW1736 细胞甲状腺肿瘤异种移植小鼠模型,并用 PL-Pt(II) 复合物进行治疗。

结果

PL-Pt(II) 复合物处理 SW1736 和 BHP7-13 细胞可剂量依赖性地降低细胞增殖,IC50 分别为 1.25µM 和 1.0µM,同时增加 G0/G1 期细胞比例,抑制 p53、cyclin D1,促进 p27 和 p21 表达,并显著增加亚 G1 期细胞比例。PL-Pt(II) 复合物处理可增加 caspase-3 的降解,降低 p-4EBP1、p-4E-BP1 和 p-S6 的表达,降低 p-ERK1/2 和 p-AKT 的表达。PL-Pt(II) 复合物治疗可减少第 14 天和第 21 天 SW1736 小鼠肿瘤异种移植物的体积,并降低 AKT 磷酸化和 S6 蛋白表达,增加 caspase-3 的降解。

结论

PL-Pt(II) 复合物对人甲状腺癌细胞的细胞毒性作用,包括激活细胞凋亡和增加细胞周期的亚 G1 细胞比例,是通过下调 mTOR 通路介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a96/7341900/d6d04445dfcf/medscimonit-26-e922561-g001.jpg

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