Conclusion
Cordycepin inhibited the proliferation and migration of gastric cancer cells by upregulating CLEC2 via the Akt signaling pathway.
Methods
The human gastric cancer cell lines MGC-803 and HGC-27 were treated with different concentrations of cordycepin (25 μM, 50 μM, 100 μM and 5 μM, 25 μM and 50 μM) for 48 h. Cell proliferation was assessed by MTT and colony formation assays, and in vitro migration by the wound healing and transwell assays. In addition, Flow Cytometry was used to detect the cell cycle and apoptosis. RT-PCR and Western blotting were used to evaluate the expression levels of key factors.
Purpose
Gastric cancer is a common malignancy worldwide, and is associated with high morbidity and mortality rates. Cordycepin is a 3'-deoxyadenosine drug with significant anti-cancer effects. The aim of this study was to determine the molecular mechanisms underlying cordycepin action on gastric cancer cell proliferation and migration.
Results
Cordycepin significantly inhibited gastric cancer cell proliferation and migration in a dose-dependent manner, in addition to inducing apoptosis and arresting the cell cycle at the G2 phase. Mechanistically, cordycepin targeted the PI3K/Akt signaling pathway by significantly altering the expression levels/activation of several key mediators, and upregulated the anti-metastatic factor CLEC2.