Cancer Biomark. 2017;18(4):329-338. doi: 10.3233/CBM-160095.
Previous studies indicate that the triterpene glycoside Actein from the herb black cohosh inhibits growth of human breast cancer cells. This study sought to investigate the effects of Actein on glioma cell growth and explore the potential mechanisms. Our results showed that administration of Actein significantly inhibited glioma cell viability in a dose- and time-dependent manner. Actein also increasingly inhibited the colony formation processes in glioma U87 cells and U251 cells. Administration of Actein also induced mitochondria-related apoptosis by increasing expression of pro-apoptotic factors Bax, cleaved caspase-3, cleaved caspase-9 and cleaved poly (ADP-ribose) polymerase 1 (PARP1) as well as decreasing anti-apoptotic Bcl-2 expression in U87 cells and U251 cells. In a xenograft model of glioma, Actein suppressed tumor growth and consistently induced cell apoptosis with the same mechanisms observed in vitro. In all, this study is the first report to address the growth inhibitory effects of Actein on glioma growth and propose that mitochondria-mediated apoptosis pathway may underlie the biological activities of Actein in glioma. Our study suggests that administration of Actein may serve as a potent therapeutic strategy for treatment of glioma.
先前的研究表明，黑升麻中的三萜糖苷 Actein 能够抑制人乳腺癌细胞的生长。本研究旨在探讨 Actein 对神经胶质瘤细胞生长的影响，并探索其潜在机制。我们的结果表明，Actein 以剂量和时间依赖的方式显著抑制神经胶质瘤细胞活力。Actein 还能逐渐抑制 U87 细胞和 U251 细胞中的集落形成过程。Actein 通过增加促凋亡因子 Bax、裂解的 caspase-3、裂解的 caspase-9 和裂解的多聚（ADP-核糖）聚合酶 1（PARP1）的表达以及降低抗凋亡 Bcl-2 的表达，诱导与线粒体相关的细胞凋亡。在神经胶质瘤的异种移植模型中，Actein 抑制肿瘤生长并通过与体外观察到的相同机制一致地诱导细胞凋亡。总之，本研究首次报道了 Actein 对神经胶质瘤生长的抑制作用，并提出线粒体介导的细胞凋亡途径可能是 Actein 在神经胶质瘤中发挥生物学活性的基础。我们的研究表明，Actein 的给药可能是治疗神经胶质瘤的一种有效治疗策略。
