由于恶性甲状腺癌（TC）的发病率和转移率不断上升，对新型抗甲状腺癌（TC）药物的需求迫切。在本研究中，我们研究了Polyphyllin VII (PPVII)对TC细胞的作用，并探讨了其潜在机制。 B-CPAP 和 TPC-1 细胞用于通过量化细胞生长和转移来分析 PPVII 的抗肿瘤活性，并研究对上皮间质转化 (EMT) 的影响。结果表明，PPVII 显着降低了 B-CPAP 和 TPC-1 细胞以剂量反应方式增殖和迁移的能力。 PPVII处理TC细胞后，E-cadherin表达量逐渐升高并高于对照组，而EMT相关基因Vimentin、N-cadherin、Slug、Zeb-1、Foxe1表达量逐渐下降，均低于对照组。有人提出 PPVII 可能会阻止 TC 接受 EMT。根据生物信息学数据库研究，Foxe1 基因在 TC 中显着表达，并且在疾病的各个临床阶段观察到 Foxe1 表达存在统计学上的显着变化。 Foxe1 基因的表达与 EMT 相关基因之间存在密切联系。同时，PPVII可抑制TC细胞Foxe1的表达。总之，我们的结果表明 PPVII 可能作为甲状腺癌 EMT 靶向治疗的潜在药物。版权所有 © 2024 作者。由 Elsevier B.V. 制作和托管。保留所有权利。

The need for novel anti-thyroid cancer (TC) medications is urgent due to the rising incidence and metastatic rates of malignant TC. In this study, we investigated the effect of Polyphyllin VII (PPVII) to TC cells, and explored their potential mechanism. B-CPAP and TPC-1 cells, were used to analyze the antitumor activity of PPVII by quantifying cell growth and metastasis as well as to study the effect on epithelial mesenchymal transition (EMT). The results showed that PPVII dramatically reduced the capacity of B-CPAP and TPC-1 cells to proliferate and migrate in a dose-response manner. Following PPVII treatment of TC cells, the expression levels of E-cadherin progressively increased and were higher than the control group, while the expression levels of EMT-related genes Vimentin, N-cadherin, Slug, Zeb-1, and Foxe1 gradually declined and were lower than the control group. It was proposed that PPVII might prevent TC from undergoing EMT. The Foxe1 gene was shown to be significantly expressed in TC, and a statistically significant variation in Foxe1 expression was observed across clinical stages of the disease, according to a bioinformatics database study. There was a strong link between the expression of the Foxe1 gene and the EMT-related gene. In the meantime, TC cells' expression of Foxe1 can be inhibited by PPVII. In conclusion, our results showed that PPVII may as a potential medication for targeting EMT in thyroid cancer.Copyright © 2024 The Authors. Production and hosting by Elsevier B.V. All rights reserved.