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首页> 外文期刊>Journal of biochemical and molecular toxicology >Scutebarbatine A induces cytotoxicity in hepatocellular carcinoma via activation of the MAPK and ER stress signaling pathways
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Scutebarbatine A induces cytotoxicity in hepatocellular carcinoma via activation of the MAPK and ER stress signaling pathways

机译：刺骨巴特巴汀通过MAPK和ER应力信号通路的激活诱导肝细胞癌中的细胞毒性

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摘要

Scutebarbatine A (SBT-A), a diterpenoid alkaloid found in the root of Scutellaria barbata D. Don, has been reported to induce the apoptosis of A549 cells. In this study, we investigated the antitumor activity of SBT-A in human hepatocellular carcinoma (HCC) cells and the potential underlying mechanisms. Our results showed that SBT-A inhibited the growth of HCC cells in a dose-dependent manner. SBT-A treatment caused cell cycle arrest and decreased the expression of cyclin B1, cyclin D1, p-Cdc2, and p-Cdc25C. SBT-A triggered cell apoptosis via a caspase-dependent pathway, and cell viability was partially restored by pretreatment with the pan-caspase inhibitor Z-VAD-FMK. In HCC cells, treatment with SBT-A increased the phosphorylation of extracellular signal-regulated kinase 1 and 2 (ERK1/2), c-Jun N-terminal kinase 1 and 2 (JNK1/2), and p38 mitogen-activated protein kinase (p38 MAPK). Moreover, SBT-A activated endoplasmic reticulum (ER) stress through the upregulation of protein kinase RNA-like ER kinase (PERK), activating transcription factor 4 (ATF-4), and CCAAT-enhancer-binding protein (C/EBP) homologous protein (CHOP). Our data indicate that SBT-A inhibits the proliferation of HCC cells and triggers their apoptosis via the activation of MAPK and ER stress. SBT-A is a potential agent for the treatment of HCC.
机译：黄芩乙素A（SBT-A）是一种二萜生物碱，存在于半枝莲根中，据报道可诱导A549细胞凋亡。在本研究中，我们研究了SBT-A在人肝细胞癌（HCC）细胞中的抗肿瘤活性及其潜在的机制。我们的结果表明，SBT-A以剂量依赖性的方式抑制肝癌细胞的生长。SBT-A治疗导致细胞周期停滞，并降低细胞周期蛋白B1、细胞周期蛋白D1、p-Cdc2和p-Cdc25C的表达。SBT-A通过半胱天冬酶依赖性途径触发细胞凋亡，并通过泛半胱天冬酶抑制剂Z-VAD-FMK预处理部分恢复细胞活力。在HCC细胞中，SBT-A治疗增加了细胞外信号调节激酶1和2（ERK1/2）、c-Jun N末端激酶1和2（JNK1/2）以及p38丝裂原激活蛋白激酶（p38 MAPK）的磷酸化。此外，SBT-A通过上调蛋白激酶RNA样内质网激酶（PERK）、激活转录因子4（ATF-4）和CCAAT增强子结合蛋白（C/EBP）同源蛋白（CHOP）来激活内质网（ER）。我们的数据表明，SBT-A通过激活MAPK和内质网应激抑制肝癌细胞的增殖并触发其凋亡。SBT-A是治疗肝癌的潜在药物。

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