Acquisition of radioresistance by IL-6 treatment is caused by suppression of oxidative stress derived from mitochondria after γ-irradiation

Interleukin (il)-6 is a multifunctional cytokine and is one of the radiation-induced bystander factors. this study aimed to clarify the mechanism of acquisition of radioresistance through the control of reactive oxygen species (ros) by il-6. we used a rat glioma cell line (c6) as tumor cells and a rat astrocyte cell line (rnb) as non-tumor cells. our results showed that the surviving fraction of c6 cells after 6 gy irradiation was increased by the addition of il-6,but that this was not the case in rnb cells. in addition,the number of 53bp1 foci in c6 cells at 30 min after γ-irradiation were decreased by il-6. levels of ros in whole c6 cells,and superoxide in the mitochondria of c6 cells immediately after γ-irradiation,were reduced by il-6,but this was not observed in rnb cells. the mitochondrial membrane potential detected by jc-1 in c6 and rnb cells was inhibited by il-6 alone. therefore,it was concluded that il-6 leads specifically to radioresistance in tumor cells by inhibition of increases in ros after γ-irradiation. © 2017 the author.