Erchen decoction plus huiyanzhuyu decoction inhibits the cell cycle, migration and invasion and induces the apoptosis of laryngeal squamous cell carcinoma cells
Erchen decoction plus huiyanzhuyu decoction inhibits the cell cycle, migration and invasion and induces the apoptosis of laryngeal squamous cell carcinoma cells
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二陈汤联合慧咽逐瘀汤抑制喉鳞状细胞癌细胞周期、迁移和侵袭并诱导其凋亡
DOI：
10.1016/j.jep.2020.112638
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发表时间：
2020-06-28
影响因子：
5.4
通讯作者：
Li, Yunying
中科院分区：
文献类型：
--
作者：
Zhou, Shiqing;Luo, Qiulan;Li, Yunying
民族药理学相关性：喉癌是头颈部最常见的恶性肿瘤之一，发病率和死亡率都很高。二陈汤合慧眼逐瘀汤是治疗LC的常用方，疗效显著。本研究的目的：探讨EHD对体外培养的人肝癌细胞株（LC）细胞周期、凋亡、迁移和侵袭的影响，并探讨其生物学机制。采用CCK-8法、显微镜、流式细胞术、EdU掺入法、Hoechst 33342染色法、伤口愈合法和transwell法分别检测EHD的抗肿瘤作用。结果：EHD处理可显著降低喉鳞状细胞癌（LSCC）细胞中STAT 3和p-STAT 3蛋白的表达水平。EHD可使细胞周期阻滞于G 0/G1期，诱导喉鳞癌细胞凋亡。EHD还能明显抑制喉鳞癌细胞的存活、迁移和侵袭能力。另外，EHD处理后细胞周期相关蛋白cyclin D1和cyclin B1的表达下调，而P27的表达上调。对于凋亡相关蛋白，EHD也降低Bcl-2的表达，但上调Box和caspase-3的表达在LSCC细胞。在迁移和侵袭相关蛋白分析中，EHD下调MMP-9的表达和上调E-cadherinexpression.Conclusions：这些结果表明，EHD在喉鳞癌中具有抗癌作用。EHD治疗可诱导喉鳞癌细胞凋亡，抑制细胞周期、迁移和侵袭，但其机制有待进一步研究。
Ethnopharmacological relevance: Laryngeal carcinoma (LC) is one of the most common malignant head and neck cancers with high incidence and mortality rates. Erchen decoction plus Huiyanzhuyu decoction (EHD) is commonly used for treating LC patients and produces beneficial results. However, the mechanisms underlying the effects of EHD remain unclear.Aim of the study: The present study aimed to analyse the anticancer effects of EHD on the LC cell cycle, apoptosis, migration and invasion in vitro and to explore the underlying biological mechanisms.Materials and methods: TU212 and Hep-2 cells were used. The antitumour effects of EHD were detected by CCK8, microscopy, flow cytometry, EdU incorporation, Hoechst 33342 staining, wound-healing, and transwell assays to assess viability, morphology, apoptosis, cell cycle, migration and invasion, respectively. Furthermore, STAT3 and related proteins were evaluated in laryngeal squamous cell carcinoma (LSCC) cells by Western blot (WB) analysis.Results: EHD treatment significantly decreased STAT3 and p-STAT3 protein expression levels in LSCC cells. EHD blocked the cell cycle at the G0/G1 phase and induced LSCC apoptosis. Moreover, the viability, migration, and invasion of LSCC cells were markedly inhibited by EHD. In addition, the expression of the cell cycle-related proteins cyclin D1 and cyclin B1 was downregulated in LSCC cells, but P27 expression was increased after EHD treatment. Regarding apoptosis-related proteins, EHD also reduced Bcl-2 expression but upregulated Box and caspase-3 expression in LSCC cells. In the migration- and invasion-related protein analyses, EHD downregulated MMP-9 expression and upregulated E-cadherin expression.Conclusions: These results suggest that EHD has an anticancer effect in LSCC. EHD treatment induces apoptosis and inhibits the cell cycle, migration and invasion of LSCC cells, but further work is warranted to address the mechanisms.