受照HaCaT细胞导致WS1旁效应细胞迁移减慢及分子机制

Increasing evidence suggests that radiation-induced bystander effects (RIBEs), which refer to the biological responses in unirradiated cells when their neighboring cells are traversed by ionizing radiation, may have an important impact on the evaluation of the health risks of ionizing radiation and the efficacy and side effects of radiotherapy for cancer patients. However, the underlying mechanisms are still unclear. In this study, we found that HaCaT cells irradiated with 0.56 Gy of α-particles and 1 Gy of X-rays showed an elevation of miR-27 expression, and after co-culture with those irradiated HaCaT cells, the unirradiated bystander WS1 cells displayed radiation-induced bystander effects such as an increase in miR-27a expression and intracelluar reactive oxygen species (ROS) levels and a slowed cell migration. Moreover, the slowed migration of bystander WS1 cells was abolished when the elevation of miR-27a expression in irradiated HaCaT cells and the increase in intracellular ROS levels in bystander WS1 cells were inhibited. On the other hand, exogenous overexpression of miR-27a in WS1 cells induced bystander-like effects, e. g. elevated ROS levels and slowed cell migration. All these data suggest that the elevation of miR-27a expression in irradiated signaling HaCaT cells is essential to the occurrence of bystander effects in unirradiated WS1 cells after co-culture, and the increase in miR-27a expression and intracellular ROS levels in bystander WS1 cells also make an important contribution to the slowed cell migration. In summary, this study has demonstrated the important regulatory effect of miR-27a on the slowed migration of bystander WS1 cells co-cultured with irradiated HaCaT cells.