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大狼毒苷 D 通过抑制 Akt/mTOR 和 STAT3 信号通路抑制三阴性乳腺癌细胞增殖。

Arnicolide D Inhibits Triple Negative Breast Cancer Cell Proliferation by Suppression of Akt/mTOR and STAT3 Signaling Pathways.

机构信息

State Key Laboratory of Chinese Medicine and Molecular Pharmacology (Incubation), Shenzhen Research Institute, The Hong Kong Polytechnic University, Shenzhen 518057, China.

Department of Applied Biology & Chemical Technology, The Hong Kong Polytechnic University, Hung Hom, Hong Kong S.A.R., China.

出版信息

Int J Med Sci. 2020 Jun 15;17(11):1482-1490. doi: 10.7150/ijms.46925. eCollection 2020.

DOI:10.7150/ijms.46925
PMID:32669950
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7359397/
Abstract

Triple-Negative Breast Cancer (TNBC) is a most dangerous breast cancer subtype. The naturally occurring sesquiterpene lactone, arnicolide D (AD), has proven effective against a variety of tumors, however, the inhibitory effects of AD against TNBC and the underlying mechanisms remain unclear. In the present study, two TNBC cell lines (MDA-MB-231 and MDA-MB-468) and an MDA-MB-231 xenograft mouse model were employed to investigate the anti-TNBC effects of AD and . Cell viability was assessed by MTT assay. Cell cycle arrest and apoptosis were analyzed by flow cytometry. Protein levels were determined by immunoblotting. studies demonstrated that AD significantly decreased cell viability, and induced G2/M cell cycle arrest and apoptosis. assays showed that oral administration of 25 or 50 mg/kg AD for 22 days led to a reduction of tumor weights by 24.7% or 41.0%, without appreciable side effects. Mechanistically, AD inhibited the activation of Akt/mTOR and STAT3 signaling pathways. Based on our findings, AD is a promising candidate for development as an adjunctive therapeutic drug for TNBC.

摘要

三阴性乳腺癌（TNBC）是一种最危险的乳腺癌亚型。天然存在的倍半萜内酯，arnicolide D（AD）已被证明对多种肿瘤有效，然而，AD 对 TNBC 的抑制作用及其潜在机制尚不清楚。在本研究中，使用了两种 TNBC 细胞系（MDA-MB-231 和 MDA-MB-468）和 MDA-MB-231 异种移植小鼠模型来研究 AD 的抗 TNBC 作用。通过 MTT 分析评估细胞活力。通过流式细胞术分析细胞周期停滞和细胞凋亡。通过免疫印迹法测定蛋白水平。研究表明 AD 显著降低细胞活力，并诱导 G2/M 细胞周期停滞和细胞凋亡。体内实验表明，口服 25 或 50mg/kg AD 22 天可使肿瘤重量分别减少 24.7%或 41.0%，而无明显副作用。机制上，AD 抑制了 Akt/mTOR 和 STAT3 信号通路的激活。基于我们的发现，AD 是作为 TNBC 辅助治疗药物开发的有前途的候选药物。

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