Abstract
Salidroside, an active ingredient extracted from the Rhodiola rosea plant, has potential anti‑tumor effects. However, the effects of salidroside on gastric cancer cell proliferation and migration remain unclear. In the present study, the inhibitory effects of salidroside on gastric cancer cell proliferation, migration and invasion and the molecular mechanisms underlying these effects were investigated. The human gastric cancer cell line, BGC‑823, was treated with different concentrations of salidroside (200, 400 and 600 µg/ml). Cell proliferation was determined with Cell Counting Kit‑8 and colony formation assays, and the migration and invasion of cells was detected by a wound healing and Transwell assay, respectively. Western blotting was performed to detect the levels of N‑cadherin, E‑cadherin and heat shock protein (HSP)70. In addition, the phosphorylation of proto‑oncogene tyrosine‑protein kinase Src (Src), protein kinase B (Akt), mitogen activated protein kinase 1 (ERK), signal transducer and activator of transcription (STAT)3 and focal adhesion kinase 1 (FAK) was examined by western blotting. The levels of matrix metalloproteinase (MMP)‑2 and MMP‑9 were determined by enzyme‑linked immunosorbent assay kits. Levels of reactive oxygen species (ROS) in cells were measured by a fluorescence plate reader with dichloro‑dihydro‑fluorescein diacetate. The results indicated that salidroside significantly suppressed cell proliferation and colony formation, inhibited cell migration and invasion, increased E‑cadherin expression and decreased N‑cadherin, MMP‑2 and MMP‑9 expression. Furthermore, salidroside suppressed ROS production and subsequently reduced the phosphorylation of Src, Akt, ERK and FAK. Salidroside also inhibited HSP70 expression, and HSP70 overexpression reversed the inhibitory effects of salidroside on BGC‑823 cell proliferation, migration and invasion. In conclusion, the present study revealed that salidroside inhibited the proliferation, migration and invasion of BGC‑823 cells by downregulating ROS‑mediated Src‑associated signaling pathway activation and HSP70 expression.