人参皂苷 Rh2 诱导 HEC1A 和 Ishikawa 子宫内膜癌细胞凋亡并抑制上皮-间充质转化。
Ginsenoside Rh2 induces apoptosis and inhibits epithelial-mesenchymal transition in HEC1A and Ishikawa endometrial cancer cells.
机构信息
Department of Obstetrics and Gynecology, Seoul National University Bundang Hospital, Seongnam, Republic of Korea.
Department of Obstetrics and Gynecology, Seoul National University Bundang Hospital, Seongnam, Republic of Korea.
出版信息
Biomed Pharmacother. 2017 Dec;96:871-876. doi: 10.1016/j.biopha.2017.09.033. Epub 2017 Nov 6.
BACKGROUND
Anticancer effect of ginsenoside Rh2 has been found in various cancer cells. However, the anticancer effect of Rh2 in endometrial cancer cells is still unclear. We aimed to determine the anticancer effect of Rh2 and elucidate its mechanism in endometrial cancer cells, using HEC1A and Ishikawa cell lines, in this study.
METHODS
Cell proliferation was assessed by MTT assay, and cell apoptosis was visualized by TdT mediated-dUTP Nick-End Labeling (TUNEL) method. Western blot were performed to detect the expression of apoptosis and epithelial-mesenchymal transition (EMT)-related proteins. Further, cell invasion and migration assays were conducted to estimate cell migration and invasion abilities.
RESULTS
Rh2 treatment significantly suppressed cell proliferation in HEC1A and Ishikawa cells, in dose-dependent manner. Levels of cleaved poly adenosine diphosphate-ribose polymerase (PARP) and cleaved caspase-3 increased in the both cell lines with Rh2 compared with control. In Western blotting analysis after Rh2 treatment, the expression of E-cadherin increased, while the expression of EMT-related proteins including vimentin, TGF-β, and Snail markedly decreased in both cell lines. The cell invasion and migration assays results indicated that Rh2 inhibited the cell invasion and migration in HEC1A cells.
CONCLUSIONS
Our findings suggested that Rh2 exerts the anticancer effect in endometrial cancer cells through the apoptosis induction and EMT inhibition.
背景
人参皂苷 Rh2 在各种癌细胞中都有抗癌作用。然而，Rh2 在子宫内膜癌细胞中的抗癌作用尚不清楚。在这项研究中，我们旨在使用 HEC1A 和 Ishikawa 细胞系确定 Rh2 的抗癌作用，并阐明其在子宫内膜癌细胞中的作用机制。
方法
通过 MTT 测定评估细胞增殖，通过 TdT 介导的 dUTP 缺口末端标记（TUNEL）法观察细胞凋亡。通过 Western blot 检测凋亡和上皮间质转化（EMT）相关蛋白的表达。进一步进行细胞侵袭和迁移实验，以评估细胞迁移和侵袭能力。
结果
Rh2 处理以剂量依赖性方式显著抑制 HEC1A 和 Ishikawa 细胞的增殖。与对照组相比，Rh2 处理后这两种细胞系中裂解的多聚腺苷二磷酸核糖聚合酶（PARP）和裂解的半胱天冬酶-3 的水平增加。在 Rh2 处理后的 Western blot 分析中，E-钙黏蛋白的表达增加，而 EMT 相关蛋白包括波形蛋白、TGF-β 和 Snail 的表达明显降低。细胞侵袭和迁移实验结果表明，Rh2 抑制了 HEC1A 细胞的侵袭和迁移。
结论
我们的研究结果表明，Rh2 通过诱导细胞凋亡和抑制 EMT 发挥对子宫内膜癌细胞的抗癌作用。
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