MECHANISM OF MIR-512-5P TO PROMOTE RADIOTHERAPY SENSITIVITY OF LUNG CANCER BY TARGETING SOD2

Hongbo Zhang¹, Jun Bao², Shaobing Li³, Liting Qian^{1, *}

¹The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230031, China - ²National Synchrotron Radiation Laboratory, University of Science and Technology of China, Hefei 230029, P.R. China - ³Department of Anatomy, College of Basic Medicine, Anhui Medical University, Hefei, Anhui, 230032, China

Objective: To investigate the effect of miR-512-5p on the radiotherapy sensitivity of lung cancer cells. 

Methods: The overexpression of miR-512-5p was performed in lung cancer cells and verified by real-time quantitative PCR. The effect of miR-512-5p on the survival rate of lung cancer cells was investigated by MTT combined cloning assay, the effect of miR-512-5p on apoptosis induced by radiotherapy was detected by flow cytometry, and the regulatory effect of miR-512-5p on the production of active oxygen cluster (ROS) induced by radiotherapy was investigated by DCF assay. Biological information analysis and luciferase reporter gene detection were used to verify the regulatory effect of miR-512-5p on manganese superoxide dismutase (SOD2). The effect of miR-512-5p on the expression of SOD2 in lung cancer cells was detected by western blot assay. Finally, the effect of miR-512-5p on the sensitivity of lung cancer cells to radiotherapy was further verified by a rescue experiment.

Results: Overexpression of miR-512-5p in A549 cells could increase the death induced by radiotherapy and apoptosis, and the overexpression of miR-512-5p could increase the ROS (p is produced by radiotherapy). MiR-512-5p could bind to the SOD2 3undefinedUTR region, thus regulating the expression of SOD2, while the overexpression of SOD2 could weaken the sensitising effect of radiotherapy induced by the overexpression of miR-512-5p.

Conclusion: miR-512-5p can increase the ROS produced via radiotherapy by inhibiting the expression of SOD2, thereby improving the sensitivity of lung cancer cells to radiotherapy.