Dysregulation of miR-711 exerts a protective role against the X-ray-induced-injury in human umbilical vein endothelial cells

Radiation therapy inevitably causes certain radiation damage to normal cells such as human vascular endothelial cells (HVECs), in addition to eliminating tumor cells. This article discusses the influence of miR-711 on the survival and apoptosis of human umbilical vein endothelial cells (HUVECs) after X-ray radiation.

The expression of miR-711 and v-maf musculoaponeurotic fibrosarcoma oncogene family protein G (MAFG) was detected by real-time quantitative polymerase chain reaction (RT-qPCR), and the content of vascular cell adhesion molecule 1 (VCAM-1) in serum was detected by Enzyme-linked immunosorbent assay (ELISA). The survival and apoptosis of HUVECs after X-ray irradiation were analyzed by functional experiments, and validation of MAFG as a miR-711 target was done by dual-luciferase reporter assay.

In the serum of prostate cancer patients miR-711 was up-regulated, while MAFG was down-regulated compared to the control group. After X-ray radiation intervention, miR-711 levels were increased, in contrast, MAFG levels decreased with a concomitant increase in VCAM-1 expression.. The percentage of survival level of HUVECs decreased gradually and the apoptosis rate of HUVECs increased as the dosage of X-ray radiation increased. Notably, after 2Gy X-ray radiation, the miR-711 inhibitor increased the survival rate of HUVECs while reducing the apoptosis rate, in contrast to the miR-711 mimic decreased the survival rate of HUVECs and increased the apoptosis. Besides, luciferase activity assay demonstrated the targeting of miR-711 to MAFG.

The inhibition of miR-711 might abrogate the function of X-ray irradiation on the survival and apoptosis of HUVECs.