Abstract
Ketamine, an anesthetic, analgesic, or sedative, is widely used for the treatment of cancer pain. Recently, ketamine has been also reported to be tumor repressor for inhibiting proliferation, invasion, and migration, and inducing apoptosis in many cancers. However, whether ketamine can induce the apoptosis of lung adenocarcinoma (LUAD) and which downstream molecular mediates its function remain largely unknown. A LUAD cell line A549 was incubated with ketamine at 0, 1, 10, and 100 μmol/L for 24 h. Trypan blue staining was used to detect the cell viability. Flow cytometry (FACS) was applied to evaluate cell apoptosis proportion. The expression of CD69 was quantitated by western blotting. Ketamine induced the A549 cell apoptosis in a concentration-dependent manner. CD69 was downregulated in LUAD patients' cancer tissue compared with the normal tissue. CD69 can be upregulated in ketamine treating A549 cells and induce the A549 cell apoptosis. Rescue experiment showed that downregulation of CD69 significantly blocked the function of ketamine on inducing apoptosis. Taken together, our results demonstrated that ketamine induced LUAD cells apoptosis by upregulating the CD69 expression. This study suggests that the ketamine can be potential drug for LUAD treatment, and the ketamine/CD69 signaling may be the new potential therapeutic target LUAD therapy.