Downregulation of eukaryotic initiation factor 4A1 improves radiosensitivity by delaying DNA double strand break repair in cervical cancer.

Expression of eukaryotic initiation factor 4A1 (eIF4A1) following brachytherapy has been reported to predict improved radiosensitivity and tumor-specific survival in cervical cancer. Therefore, the present study investigated the function of eIF4A1 in cervical cancer and the mechanism by which eIF4A1 regulates cervical cancer radiosensitivity. It was determined that the downregulation of eIF4A1 in HeLa and SiHa cells notably attenuated cell proliferation, in addition to repressing cervical cancer migration and invasion, and promoting cell apoptosis. In vitro and in vivo studies have demonstrated that silencing eIF4A1 improves cervical cancer radiosensitivity. Detection of γ-H2AX using western blot analysis at 0, 0.5, 1, 6 and 24 h following the exposure of cervical cancer cells to X-rays illustrated that eIF4A1-knockdown results in postponed radiation-induced DNA double strand break (DSB) repair. Overall, the results of the present study demonstrated that downregulated eIF4A1 improves cervical cancer radiosensitivity by delaying cancer cell DSB repair. In conclusion, the data indicated that eIF4A1 performs a vital role in cervical cancer progression and radiosensitivity. Therefore, eIF4A1 may be a potential therapeutic target in patients with cervical cancer.