口腔癌是一种常见的肿瘤，严重影响人们的健康，甚至导致死亡。黄芪甲苷 IV (AS-IV) 是黄芪提取物的主要成分之一，已被确定对某些癌症具有改善功能。然而，AS-IV 在口腔癌中的监管影响和相关途径仍然模糊。本研究发现，随着AS-IV剂量（25、50和100μM）的增加，细胞生长逐渐减弱。此外，还发现 AS-IV 抑制了口腔癌的 EMT 进展。 AS-IV处理后细胞迁移和侵袭能力均逐渐减弱，且呈剂量依赖性。此外，AS-IV通过增强LC3II/LC3I水平和LC3B荧光强度来加速自噬。最后阐明AS-IV触发AMPK通路并阻滞AKT/mTOR通路。总之，AS-IV 通过调节 AMPK 和 AKT/mTOR 通路加剧自噬，从而抑制口腔癌的细胞增殖、迁移、侵袭和上皮间质转化 (EMT) 进展。这项工作可能为 AS-IV 治疗口腔癌提供新的证据。版权所有 © 2024 Elsevier Ltd. 保留所有权利。

Oral cancer is one usual tumor that sorely affects the health of people and even result into death. Astragaloside IV (AS-IV) is one of the major components of Astragalus membranaceus extract, and has been identified to exhibit ameliorative functions in some cancers. Nevertheless, the regulatory impacts and correlative pathways of AS-IV in oral cancer remain vague. In this study, it was discovered that cell growth was gradually weakened with the increased dose of AS-IV (25, 50 and 100 μM). Additionally, it was uncovered that AS-IV restrained the EMT progress in oral cancer. The cell migration and invasion abilities were both gradually alleviated after AS-IV treatment in a dose-dependent manner. Moreover, AS-IV accelerated autophagy through intensifying LC3II/LC3I level and LC3B fluorescence intensity. At last, it was clarified that AS-IV triggered the AMPK pathway and retarded the AKT/mTOR pathway. In conclusion, AS-IV restrained cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) progress in oral cancer by aggravating autophagy through modulating the AMPK and AKT/mTOR pathways. This work may offer novel evidence on AS-IV in the treatment of oral cancer.Copyright © 2024 Elsevier Ltd. All rights reserved.