Metformin enhances radiation response of ECa109 cells through activation of ATM and AMPK

Metformin is a first-line used agent for type II diabetes with few side effects. The antineoplastic effect of metformin was widely explored recently. Metformin may also be a prospective chemosensitizer or radiosensitizer in cancer treatment. In the present study, we firstly showed that metformin could effectively enhance the anti-proliferation effect of ionizing radiation (IR) on esophageal cancer (EC) cells ECa109. More potent DNA damage was observed by detection of γH2AX foci. Metformin synergistically induce apoptosis and cell cycle arrest in ECa109 cells with IR. Furthermore, the mechanisms how metformin sensitized ECa109 cells to IR may be targeting the ATM and AMPK/mTOR/HIF-1α pathways. Metformin may be a valuable agent in comprehensive treatment of EC.