摘要
This study explored the role of radiation-induced autophagy in low-dose hyperradiosensitiv- ity （HRS） in the human lung cancer cell line A549. A549 cells, either treated with an autophagic inhibitor 3-methyladenine （3-MA）, or with a vehicle control, were irradiated at different low doses （〈0.5 Gy）. The generation of autophagy was examined by laser scanning confocal microscopy. Western blot- ting was used to detect the expression ofmicrotubule-associated protein I light chain 3B II （LC3B- II）. Flow cytometry （FCM） and clonogenic assays were used to measure the fraction of surviving cells at the low irradiation doses. Our results showed that there was a greater inhibition of autophagic activity, but a higher degree of low-dose HRS in A549 cells treated with 3-MA than in control group. Our data dem- onstrated that radiation-induced autophagy is correlated with HRS in A549 cells, and is probably one of the mechanisms underlying HRS.
This study explored the role of radiation-induced autophagy in low-dose hyperradiosensitiv- ity （HRS） in the human lung cancer cell line A549. A549 cells, either treated with an autophagic inhibitor 3-methyladenine （3-MA）, or with a vehicle control, were irradiated at different low doses （〈0.5 Gy）. The generation of autophagy was examined by laser scanning confocal microscopy. Western blot- ting was used to detect the expression ofmicrotubule-associated protein I light chain 3B II （LC3B- II）. Flow cytometry （FCM） and clonogenic assays were used to measure the fraction of surviving cells at the low irradiation doses. Our results showed that there was a greater inhibition of autophagic activity, but a higher degree of low-dose HRS in A549 cells treated with 3-MA than in control group. Our data dem- onstrated that radiation-induced autophagy is correlated with HRS in A549 cells, and is probably one of the mechanisms underlying HRS.
基金
supported by the National Natural Science Foundation of China (No.30900383)
