Department of Vascular Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province 710061, People's Republic of China.
National Local Joint Engineering Research Center for Precision Surgery and Regenerative Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province 710061, People's Republic of China.
Int J Med Sci. 2021 Jan 1;18(1):81-87. doi: 10.7150/ijms.48552. eCollection 2021.
Oridonin, derived from , has exhibited anticancer activity in a variety of cancers. However, few studies have explored the effect of oridonin (ORI) on migration, invasion and epithelial-mesenchymal transition (EMT) in nasopharyngeal carcinoma. In our study, the results demonstrated that oridonin significantly inhibited migration and invasion of human nasopharyngeal carcinoma CNE-2Z and HNE-1 cell lines, as depicted by wound healing and Transwell assays. In addition, oridonin increased the expression of E-Cadherin while decreased the expressions of vimentin and twist1 at the mRNA and protein levels in a dose-dependent manner. Interestingly, oridonin also decreased cell mobility in nasopharyngeal carcinoma. The subsequent results of western blotting uncovered that the phosphorylation levels of AKT and signal transducer and activator of transcription 3 (STAT3) were decreased upon oridonin treatment. Furthermore, co-treatment with the AKT activator SC-79 attenuated the anti-metastatic effect of oridonin on nasopharyngeal carcinoma and partially abolished the high expression of E-cadherin and the low expression of twist1 mediated by oridonin. In conclusion, the results revealed that oridonin could repress metastatic phenotype and reverse epithelial-mesenchymal transition (EMT) in nasopharyngeal carcinoma by negatively regulating AKT/STAT3 signaling pathway, suggesting that AKT/STAT3 signaling may be the potential therapeutic target of oridonin against nasopharyngeal carcinoma.
冬凌草甲素来源于 ，在多种癌症中表现出抗癌活性。然而，很少有研究探讨冬凌草甲素（ORI）对鼻咽癌迁移、侵袭和上皮间质转化（EMT）的影响。在我们的研究中，结果表明冬凌草甲素显著抑制人鼻咽癌 CNE-2Z 和 HNE-1 细胞系的迁移和侵袭，划痕愈合和 Transwell 分析显示。此外，冬凌草甲素呈剂量依赖性增加 E-钙黏蛋白的表达，同时降低波形蛋白和 twist1 的 mRNA 和蛋白水平的表达。有趣的是，冬凌草甲素也降低了鼻咽癌细胞的迁移能力。Western blot 的后续结果显示，冬凌草甲素处理后 AKT 和信号转导和转录激活因子 3（STAT3）的磷酸化水平降低。此外，AKT 激活剂 SC-79 的共同处理减弱了冬凌草甲素对鼻咽癌的抗转移作用，并部分消除了冬凌草甲素介导的 E-钙黏蛋白高表达和 twist1 低表达。总之，结果表明冬凌草甲素通过负调控 AKT/STAT3 信号通路抑制鼻咽癌的转移表型和逆转上皮间质转化（EMT），提示 AKT/STAT3 信号通路可能是冬凌草甲素治疗鼻咽癌的潜在靶点。
