CLDR could influence the proliferation of cells via MAPK signal transduction. One representive VX-680 of two experiments is shown. Table 3 Expression changes of EGFR and Raf

in CL187 cells after irradiation and/or EGFR monoclonal antibody treatment (%, ± s).   EGFR Raf Control 45.36 ± 3.91 39.57 ± 3.48 125I irradiation 74.27 ± 5.63a 53.84 ± 2.31d Anti-EGFR mAb 2.31 ± 0.19b 14.68 ± 1.35e 125I irradiation + Anti-EGFR mAb 2.27 ± 0.13c 13.74 ± 1.82f Compared with control group (EGFR), t = 54.84,aP < 0.01; t = 27.38,bP < 0.05. Compared with anti-EGFR mAb group (EGFR), t = 1.21,cP > 0.05. Compared with control group (Raf), t = 46.66,dP < 0.01; and t = 26.60,eP < 0.01. Compared with anti-EGFR mAb group (Raf), t = 0.98,fP > 0.05. Discussion Low-energy radioactive seed TSA HDAC interstitial implantation has resulted in positive clinical treatment of many tumors previously radioresistant to high dose rate irradiation. This may be due to different

radiobiological mechanisms between low and high dose rate irradiation. Nevertheless, compared with springing up of radioactive seeds NSC23766 concentration interstitial implantation, fundamental research on this topic is notably absent, and the radiobiological mechanism of125I seed low dose rate irradiation remains unclear. As classic methods of appraising killing efficacy of irradiation, cell proliferation and clonic assays were used in the experiment. High dose rate irradiation killed tumor cells, but simultaneously induced radioresistance. the However, the dose survival curve of125I seed continuous low dose rate irradiation had no significant shoulder region, and SF was lower than60Co γ ray high dose rate irradiation. From the radiobiological parameter results, we also observed that125I continuous low dose rate

irradiation showed great advantages relative to high dose rate irradiation. Although RBE could be affected by many factors, such as cell line and dose rate, most studies have shown that the RBE of125I was between 1.3 and 1.5. The present results are consistent with previous reports [24–27]. Our results indicated that apoptosis may play a central role regarding the observed killing effects when cells were exposed to125I seed low dose rate irradiation [28, 29]. Prior studies have suggested that radiosensitivity is cell cycle dependent, and cells in the G2/M phase could be more radioresponsive [30]. These results suggest that CLDR may enhance radiosensitivity by inducing accumulation of cells in a more radiosensitive cell cycle phase (G2/M) [31, 32]. The apoptosis index of 10 Gy was lower than that of 5 Gy; two possibilities for this occurrence are: (a) Early-apoptotic cells disintegrated within the exposure time of 10 Gy, and could not be detected by FCM; and (b) Low dose rate irradiation only delayed the cell cycle, but could not completely block the cell cycle. Overshoot early irradiation, cells changed to be more radioresistant.