文献类型：期刊文献

英文题名：Raddeanoside R13 Inhibits Proliferation, Invasion, and Metastasis of Gastric Cancer Cells Based on Network Pharmacology and Experimental Validation

作者：Zhao, Tiantian[1];Wu, Qiong[2];Da, Mingxu[1,2,3];Zhu, Chenglou[1,2,3]

第一作者：赵婷婷

通信作者：Zhu, CL[1];Zhu, CL[2]

机构：[1]Gansu Univ Chinese Med, Sch Clin Med 1, Lanzhou 730000, Peoples R China;[2]Lanzhou Univ, Sch Clin Med 1, Lanzhou 730000, Peoples R China;[3]Gansu Prov Hosp, Dept Surg Oncol, Lanzhou 730000, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Lanzhou Univ, Sch Clin Med 1, Lanzhou 730000, Peoples R China;[2]corresponding author), Gansu Prov Hosp, Dept Surg Oncol, Lanzhou 730000, Peoples R China.

年份：2025

外文期刊名：CURRENT CANCER DRUG TARGETS

收录：;Scopus(收录号：2-s2.0-105010111866);WOS:【SCI-EXPANDED(收录号:WOS:001522212300001)】；

基金：This work was supported by the Natural Science Foundation of Gansu Province, China(Grant number 23JRRA1317).

语种：英文

外文关键词：Gastric cancer; raddeanoside R13; invasion; metastasis; epithelial-mesenchymal transition

摘要：Objective This study aims to explore the potential mechanisms by which Raddeanoside R13 (R13) inhibits the proliferation, invasion, and metastasis of gastric cancer (GC) cells through network pharmacology analysis and experimental validation.Methods First, network pharmacology was used to explore the potential mechanisms of R13 in treating GC. The effects of R13 on GC cell proliferation were assessed using CCK-8 and colony formation assays. Apoptosis was measured by flow cytometry, while the effects of R13 on invasion and metastasis were evaluated through wound healing and Transwell invasion assays. Finally, Western blotting was performed to investigate the impact of R13 on the expression of epithelial-to-mesenchymal transition (EMT) markers, PI3K/AKT signaling pathway proteins, and apoptosis-related proteins in GC cells.Results A total of 58 potential targets of R13 in the treatment of GC were identified. R13 was found to affect the development of GC by regulating pathways, such as NFKB1, mTOR, apoptosis, and the PI3K-AKT signaling pathway. In vitro experiments confirmed that R13 inhibited the proliferation, invasion, and metastasis of GC cells while promoting apoptosis. Additionally, we found that R13 suppressed the EMT of GC cells and reduced the phosphorylation levels of PI3K, AKT, and mTOR. When this pathway was activated, it partially reversed these effects.Conclusion R13 inhibited the proliferation, invasion, and metastasis of GC cells while inducing apoptosis. Furthermore, R13 may suppress the EMT process in GC cells by inhibiting the PI3K/AKT/mTOR signaling pathway. These findings provide a foundation for the potential use of R13 as a therapeutic strategy for GC.