摘要
AIM:To determine the mechanism of the radiationinduced biological effects of 125I seeds on pancreatic carcinoma cells in vitro.METHODS:SW1990 and PANC-1 pancreatic cancer cell lines were cultured in DMEM in a suitable environment.Gray’s model of iodine-125(125I)seed irradiation was used.In vitro,exponential phase SW1990,and PANC-1cells were exposed to 0,2,4,6,and 8 Gy using 125I radioactive seeds,with an initial dose rate of 12.13c Gy/h.A clonogenic survival experiment was performed to observe the ability of the cells to maintain their clonogenic capacity and to form colonies.Cell-cycle and apoptosis analyses were conducted to detect the apoptosis percentage in the SW1990 and PANC-1 cells.DNA synthesis was measured via a tritiated thymidine(3H-Td R)incorporation experiment.After continuous low-dose-rate irradiation with 125I radioactive seeds,the survival fractions at 2 Gy(SF2),percentage apoptosis,and cell cycle phases of the SW1990 and PANC-1 pancreatic cancer cell lines were calculated and compared.RESULTS:The survival fractions of the PANC-1 andSW1990 cells irradiated with 125I seeds decreased exponentially as the dose increased.No significant difference in SF2 was observed between SW1990 and PANC-1 cells(0.766±0.063 vs 0.729±0.045,P<0.05).The 125I seeds induced a higher percentage of apoptosis than that observed in the control in both the SW1990and PANC-1 cells.The rate of apoptosis increased with increasing radiation dosage.The percentage of apoptosis was slightly higher in the SW1990 cells than in the PANC-1 cells.Dose-dependent G2/M cellcycle arrest was observed after 125I seed irradiation,with a peak value at 6 Gy.As the dose increased,the percentage of G2/M cell cycle arrest increased in both cell lines,whereas the rate of DNA incorporation decreased.In the 3H-Td R incorporation experiment,the dosimetry results of both the SW1990 and PANC-1cells decreased as the radiation dose increased,with a minimum at 6 Gy.There were no significant differences in the dosimetry results of the two cell lines when t
AIM:To determine the mechanism of the radiationinduced biological effects of 125I seeds on pancreatic carcinoma cells in vitro.METHODS:SW1990 and PANC-1 pancreatic cancer cell lines were cultured in DMEM in a suitable environment.Gray’s model of iodine-125(125I)seed irradiation was used.In vitro,exponential phase SW1990,and PANC-1cells were exposed to 0,2,4,6,and 8 Gy using 125I radioactive seeds,with an initial dose rate of 12.13c Gy/h.A clonogenic survival experiment was performed to observe the ability of the cells to maintain their clonogenic capacity and to form colonies.Cell-cycle and apoptosis analyses were conducted to detect the apoptosis percentage in the SW1990 and PANC-1 cells.DNA synthesis was measured via a tritiated thymidine(3H-Td R)incorporation experiment.After continuous low-dose-rate irradiation with 125I radioactive seeds,the survival fractions at 2 Gy(SF2),percentage apoptosis,and cell cycle phases of the SW1990 and PANC-1 pancreatic cancer cell lines were calculated and compared.RESULTS:The survival fractions of the PANC-1 andSW1990 cells irradiated with 125I seeds decreased exponentially as the dose increased.No significant difference in SF2 was observed between SW1990 and PANC-1 cells(0.766±0.063 vs 0.729±0.045,P<0.05).The 125I seeds induced a higher percentage of apoptosis than that observed in the control in both the SW1990and PANC-1 cells.The rate of apoptosis increased with increasing radiation dosage.The percentage of apoptosis was slightly higher in the SW1990 cells than in the PANC-1 cells.Dose-dependent G2/M cellcycle arrest was observed after 125I seed irradiation,with a peak value at 6 Gy.As the dose increased,the percentage of G2/M cell cycle arrest increased in both cell lines,whereas the rate of DNA incorporation decreased.In the 3H-Td R incorporation experiment,the dosimetry results of both the SW1990 and PANC-1cells decreased as the radiation dose increased,with a minimum at 6 Gy.There were no significant differences in the dosimetry results of the two cell lines when t
基金
Supported by Natural Science Foundation of China,No.81271682(partly)
grants from Science and Technology Commission of Shanghai Municipality,No.11JC1407400(partly)
the project of Luwan District Science and Technology Commission of Shanghai,No.LKW1104(partly)
the project of Medical Key Specialty of Shanghai Municipality,No.ZK2012A20(partly)
