Radiosensitivity enhancement by arsenic trioxide in conjunction with hyperthermia in the EC-1 esophageal carcinoma cell line.

To explore the effect on radiosensitivity of arsenic trioxide (As₂0₃) in conjunction with hyperthermia on the esophageal carcinoma EC-1 cell line. Inhibition of EC-1 cell proliferation at different concentrations of As₂0₃ was assessed using the methyl thiazolyl blue colorimetric method (MTT method), with calculation of IC₅₀ value and choice of 20% of the IC₅₀ as the experimental drug concentration. Blank control, As₂0₃, hyperthermia, radiotherapy group, As₂0₃ + hyperthermia, As₂0₃ + radiotherapy, hyperthermia + radiotherapy and As₂0₃ + hyperthermia + radiotherapy groups were established, and the cell survival fraction (SF) was calculated from flat panel colony forming analysis, and fitted by the 'multitarget click mathematical model'. Flow cytometry (FCM) was used to detect changes in cell apoptosis and the cell cycle. As₂0₃ exerted inhibitory effects on proliferation of esophageal carcinoma EC-1 cells, with an IC₅₀ of 18.7 μmol/L. After joint therapy of As₂0₃ + hyperthermia + radiotherapy, the results of FCM showed that cells could be arrested in the G₂/M phase, and as the ratio of cells in G₀/G₁ and S phases decreased, cell death became more pronounced. As₂0₃ and hyperthermia exert radiosensitivity effects on esophageal carcinoma EC-1 cells, with synergy in combination. Mechanistically, As₂0₃ and hyperthermia mainly influence the cell cycle distribution of EC-1 esophageal carcinoma cells, decreasing the repair of sublethal damage and inducing apoptosis, thereby enhancing the killing effects of radioactive rays.