Ginsenoside Rg3 alleviates the migration, invasion, and angiogenesis of lung cancer cells by inhibiting the expressions of cyclooxygenase‐2 and vascular endothelial growth factor

Lung cancer (LC) is a common cancer with high incidence and mortality rates. In recent years, ginsenoside Rg3 (Rg3), a traditional medicine, is widely used for the treatment of LC. Herein, we concentrate on assessing the effect of Rg3 on LC cell migration and invasion. The effects of Rg3 (0, 25, 50, and 100 μg/ml) on the viability, migration, invasion, angiogenesis, and expressions of epithelial–mesenchymal transition (EMT)‐related proteins, cyclooxygenase‐2 (COX2), and vascular endothelial growth factor (VEGF) of LC cell lines were evaluated by cell counting kit‐8 (CCK‐8), scratch, transwell, tube formation, and western blot assays. Quantitative real‐time polymerase chain reaction (qRT‐PCR) was performed to assess transfection efficiency. COX2 overexpression plasmid and short hairpin RNA for VEGF (shVEGF) were applied to evaluate whether the effect of Rg3 is related to COX2 and VEGF through rescue assay. In this study, Rg3 significantly dose‐dependently suppressed the viability, migration, invasion, angiogenesis, and protein expressions of N‐cadherin, vimentin, COX2, and VEGF in H1299 and A549 cells, while promoting the expression of E‐cadherin protein. COX2 overexpression markedly reversed the effects of Rg3 on the viability, migration, invasion, angiogenesis, and EMT‐related protein expression levels in LC cells; however, such effects of COX2 overexpression were offset by VEGF knockdown. In sum, Rg3 alleviates the migration, invasion, and angiogenesis of LC cells by inhibiting the expressions of COX2 and VEGF. Ginsenoside Rg3 (Rg3) has an indispensable role in the curative functions of ginseng extract. Rg3 has many pharmacology actions and efficacies as natural product, including antitumor, angiogenesis, and metastasis. Rg3 alleviates the epithelial–mesenchymal transition and angiogenesis of lung cancer cells by inhibiting the expressions of COX2 and VEGF.