Xie Xiaodong, Zhu Haitao, Zhang Jia, Wang Meiqin, Zhu Li, Guo Zhen, Shen Wenrong, Wang Dongqing
Department of Radiology, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, Nanjing Medical University Affiliated Cancer Hospital, Nanjing, Jiangsu 210000, P.R. China.
Department of Radiology, The Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu 212013, P.R. China.
Oncol Lett. 2017 Jul;14(1):447-452. doi: 10.3892/ol.2017.6147. Epub 2017 May 10.
Solamargine (SM), a steroidal alkaloid glycoside purified from the Chinese traditional herb , is known to possess various biological activities. However, only a few previous studies have reported the anti-metastatic activity of SM. In the present study, the inhibitory effects of SM on metastatic action were investigated in human HepG2 cells. The proliferation effects of SM on the HepG2 cells was evaluated by MTT and colony formation assays. Wound-healing and Transwell assays were performed to examine the migration and invasion effects on SM-treated HepG2 cells. The epithelial-to-mesenchymal transition (EMT)-associated markers (E-cadherin, Vimentin and N-cadherin) were detected by western blotting analysis. In the present study, MTT and colony formation assays indicated that SM suppressed HepG2 cell viability in a dose-dependent manner. The wound-healing and Transwell assays revealed that the migration and invasion activities were significantly inhibited following exposure to SM. EMT has been demonstrated to be essential for promoting migration and invasion in tumor cells and has often been characterized with a loss of epithelial markers (E-cadherin) and an increase of mesenchymal markers (Vimentin and N-cadherin). In the western blotting analysis, the expression level of E-cadherin was significantly upregulated compared with that in the control group, whereas the expression levels of N-cadherin and Vimentin were downregulated. Thus, it was suggested that the underlying mechanism of SM inhibits migration and invasion in HepG2 cells and is associated with suppression of EMT.
龙葵碱(SM)是一种从传统中药中提纯的甾体生物碱糖苷,已知具有多种生物活性。然而,之前仅有少数研究报道过SM的抗转移活性。在本研究中,我们研究了SM对人肝癌细胞系HepG2转移作用的抑制效果。通过MTT法和集落形成实验评估了SM对HepG2细胞的增殖作用。进行了划痕实验和Transwell实验以检测SM处理后的HepG2细胞的迁移和侵袭效果。通过蛋白质免疫印迹分析检测上皮-间质转化(EMT)相关标志物(E-钙黏蛋白、波形蛋白和N-钙黏蛋白)。在本研究中,MTT法和集落形成实验表明SM以剂量依赖的方式抑制HepG2细胞活力。划痕实验和Transwell实验显示,暴露于SM后,迁移和侵袭活性受到显著抑制。EMT已被证明对促进肿瘤细胞的迁移和侵袭至关重要,其特征通常是上皮标志物(E-钙黏蛋白)的丧失和间质标志物(波形蛋白和N-钙黏蛋白)的增加。在蛋白质免疫印迹分析中,与对照组相比,E-钙黏蛋白的表达水平显著上调,而N-钙黏蛋白和波形蛋白的表达水平下调。因此,提示SM抑制HepG2细胞迁移和侵袭的潜在机制与抑制EMT有关。