Kong Yanjie, Li Fubin, Nian Yin, Zhou Zhongmei, Yang Runxiang, Qiu Ming-Hua, Chen Ceshi
1. Key Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan, 650223, China;; 2. Kunming College of Life Science, University of Chinese Academy of Sciences, Kunming 650204 Yunnan, China;
1. Key Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan, 650223, China;; 3. State Key Laboratory of Phytochemistry and Plant Resources in West China, Kunming Institute of Botany, Chinese Academy of Science, Kunming 650204 Yunnan, China;
Theranostics. 2016 Apr 12;6(6):875-86. doi: 10.7150/thno.14694. eCollection 2016.
Triterpenoids extracted from Cimicifuga foetida have been reported to inhibit cancer by inducing cell cycle arrest and apoptosis. In this study, KHF16 (24-acetylisodahurinol-3-O-β-D-xylopyranoside), a cycloartane triterpenoid isolated from the rhizomes of C. foetida, showed potent anti-cancer activity in multiple ERα/PR/HER2 triple-negative breast cancer (TNBC) cell lines. KHF16 significantly induces cell cycle G2/M phase arrest and apoptosis in both MDA-MB-468 and SW527 TNBC cell lines. KHF16 reduces the expression levels of XIAP, Mcl-1, Survivin and Cyclin B1/D1 proteins. Importantly, KHF16 inhibits TNFα-induced IKKα/β phosphorylation, IKBα phosphorylation, p65 nuclear translocation and NF-κB downstream target gene expression, including XIAP, Mcl-1 and Survivin, in TNBC cells. These results suggest that KHF16 may inhibit TNBC by blocking the NF-κB signaling pathway in part.
据报道，从升麻中提取的三萜类化合物可通过诱导细胞周期停滞和凋亡来抑制癌症。在本研究中，从升麻根茎中分离出的环阿尔廷烷三萜类化合物KHF16（24-乙酰异达胡醇-3-O-β-D-吡喃木糖苷）在多种雌激素受体α/孕激素受体/人表皮生长因子受体2三阴性乳腺癌（TNBC）细胞系中显示出强大的抗癌活性。KHF16在MDA-MB-468和SW527 TNBC细胞系中均显著诱导细胞周期G2/M期停滞和凋亡。KHF16降低了X连锁凋亡抑制蛋白（XIAP）、髓细胞白血病-1（Mcl-1）、生存素和细胞周期蛋白B1/D1的表达水平。重要的是，KHF16在TNBC细胞中抑制肿瘤坏死因子α（TNFα）诱导的IKKα/β磷酸化、IκBα磷酸化、p65核转位以及核因子κB（NF-κB）下游靶基因的表达，包括XIAP、Mcl-1和生存素。这些结果表明，KHF16可能部分通过阻断NF-κB信号通路来抑制TNBC。
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