miR-200c Modulates the Pathogenesis of Radiation-Induced Oral Mucositis

Figure 6

The potential role of miR-200c in regulating the pathogenesis of RIOM. miR-200c promoted radiation-induced NF-κB signaling by increasing the phosphorylation level of IκBα at the position ser32 and phosphorylation at position ser536 of p65 as well as nuclear translocation level, which led to overproduction of proinflammatory cytokines. miR-200c increased the DNA DSB level and ROS generation induced by radiation and caused more severe senescence phenotype. miR-200c decreased the expression of Bmi-1 and Zeb1, which led to downregulation of p-GSK-3β and Snail, thus inhibited NHK cell EMT. miR-200c mediated increased inflammation, DNA DSB, and ROS generation as well as decreased EMT capacity of NHK during the pathogenesis of RIOM.