Ginsenoside compound K inhibits the proliferation, migration and invasion of Eca109 cell via VEGF-A/Pi3k/Akt pathway

Objective Esophageal cancer, one of the most common cancers in the upper digestive tract and is one of the leading cancer-related mortality worldwide. Accumulating studies found that Ginsenoside compound K (CK) has significantly anti-tumor effects, especially in the suppression of proliferation, migration, as well as invasion in various human cancers. While the effects of Ginsenoside CK in esophageal cancer have not been well studied. In our present study, we aim to explore the functions and mechanisms of Ginsenoside CK in the progression of esophageal cancer cells (Eca109). Methods Cell Counting Kit-8 (CCK-8), wound healing, transwell and flow cytometry assays were applied to analyze the effects of Ginsenoside CK in the progression of Eca109 cell, western blot assay was used to investigate the potential downstream signaling pathway after Ginsenoside CK treatment. Results Our study found that Ginsenoside CK can suppress cell proliferation, migration and invasion of Eca109 cell. Furthermore, the flow cytometry showed that Ginsenoside CK increased of apoptosis rates in Eca109 cell. The western blot results indicated that Ginsenoside CK decreased the expression of VEGF-A, P-Pi3k and P-Akt proteins. Moreover, the knockdown of VEGF-A gene could suppress cell proliferation, migration, invasion and induce apoptosis in Eca109 cell, and the expression of P-Pi3k and P-Akt proteins were significantly downregulated. Conclusions Our study suggests that Ginsenoside CK inhibits the proliferation, migration, invasion, and induced apoptosis of Eca109 cell by blocking VEGF-A/Pi3k/Akt signaling pathway.