The histone deacetylase inhibitor CG-745 enhances the radiosensitivity of prostate cancer cells

Objective To investigate the possible correlation between histone deacetylase inhibition and radiosensitivity in PC-3 prostate cancer cells and to explore the possible mechanism involved. Methods PC-3 prostate cancer cells were treated with 0.40 μM CG-745 alone, radiation alone, or 0.40 μM CG-745 in combination with radiation. A CCK-8 kit was used to measure the proliferation of PC-3 cells. The colony formation assay was used to determine cell reproductive survival. Immunofluorescence analysis was used to detect the location of phosphorylated H2AX foci. Apoptosis and cell cycle distribution of PC-3 cells were assessed via flow cytometry analysis. Results CG-745 enhances the repressive effect of irradiation on PC-3 cell growth, as shown by the CCK-8 assay and colony formation assay. Compared with CG-745 or radiation alone, CG-745 combined with radiation significantly increased phosphorylated H2AX foci formation. The combination of CG-745 and radiation significantly increased the percentage of cells in the S phase and decreased percentage of cells in the G2 and G1 phases compared with treatment with CG-745 alone or radiation alone. Flow cytometry analysis showed that CG-745 promoted the PC-3 cell apoptosis induced by radiation. Conclusions The histone deacetylase inhibitor CG-745 enhanced radiation-induced DNA damage, cell cycle arrest, and cell apoptosis, thus increasing the radiosensitivity of PC-3 prostate cancer cells to X-ray irradiation.