Raddeanoside R13 Inhibits Proliferation, Invasion, and Metastasis of Gastric Cancer Cells Based on Network Pharmacology and Experimental Validation.

[OBJECTIVE] This study aims to explore the potential mechanisms by which Rad-deanoside 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 gastric cancer. 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 phos-phorylation 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 in-ducing apoptosis. Furthermore, R13 may suppress the EMT process in GC cells by inhibit-ing the PI3K/Akt/mTOR signaling pathway. These findings provide a foundation for the potential use of R13 as a therapeutic strategy for gastric cancer.