PRJNA725505
The role and mechanism of ATM-mediated autophagy in the transition from hyperradiosensitivity to induced radioresistance in lung cancer under low-dose radiation
Radiotherapy resistance and damage to surrounding normal tissue during radiotherapy limit its application in clinical practice. Some tumor cells exhibit hyperradiosensitivity (HRS) to low-dose radiation and few studies have focused on the mechanism of HRS in tumor cells. In the present study, ATM may influence autophagy through p-JNK and AMBRA1 to participate in the regulation of the HRS/IRR phenomenon. Autophagy interacts with the cellular carbon metabolite DL-norvaline to participate in regulating the low-dose radiosensitivity of cells.