The effect of silencing XRCC2 gene combined with ionizing radiation on growth of colorectal cancer cells

Abstract

Objective To investigate the effect of silencing X-ray repair cross complementary gene 2 (XRCC2) through shRNA interference on the radiosensitivity of colorectal cancer cells. Methods The growth of colorectal cancer T84 cells of silencing XRCC2 was determined with MTT assay and the growth inhibition rate of T84 cells was detected. The ability to form colonies of T84 cells after exposure to X-ray radiation was examined with colony formation assay. The cell cycle distribution or cell apoptosis of T84 cells irradiated with X-ray radiation was performed by flow cytometric analysis. Results The cell growth of shRNA-XRCC2 group slowed down markedly from the third day of cell culture and the growth inhibition rate of shRNA-XRCC2 group steadily maintained about 50%, which was significantly less than that of shRNA-SC group (t=17.62, 12.84, 9.24, all P<0.05) . The number of colonies formed in shRNA-XRCC2 cells and 8 Gy radiation cells was 422.7±43.4 and 389.5±24.4 respectively. The number of colonies in shRNA-XRCC2+8 Gy radiation group was the least (223.3±32.9) , which was decreased significantly compared with that of shRNA-XRCC2 group or 8 Gy group (t=8.96 and 9.92, both P<0.01) . Cells of shRNA-XRCC2 group arrested at G2/M phase were increased, reached (38.51±4.15) %, significantly higher than that of control group (t=3.92, P<0.05) . Cells apoptosis ratio of shRNA-XRCC2 group cells was the highest, reached (33.16±2.69) %, and there were significant differences compared with that of control (t=15.31, P<0.01) . Conclusion Knockdown of XRCC2 inhibited effectively the growth of colorectal cancer T84 cells in vitro. Silencing XRCC2 combined with radiation led to T84 cells arrested at G2/M phase and cells apoptosis and rendered T84 cells more sensitive to radiation. Key words: Radiation; Colonic neoplasms; RNA interference; X-ray repair cross complementing gene 2