Fig. 7
From: Rho family GTPase 1 (RND1), a novel regulator of p53, enhances ferroptosis in glioblastoma
RND1 promoted the anti-GBM activity of Erastin in vitro. A RND1 overexpression combined with Erastin significantly suppressed the growth of U87 cells. Cell viability was detected using CCK-8. B U87 cells were transfected with Flag or Flag-RND1 plasmids and treated with Erastin (10 μM). Western blot analysis was used to determine the levels of SLC7A11 and p53. C–E RND1 overexpression combined with Erastin significantly decreased the concentration of GSH and increased the level of ROS and MDA in U87 cells. F Transfected U87 cells were treated with Erastin (10 μM) and prepared for transmission electron microscopy observation. G Mechanistic model for RND1 regulation of cell ferroptosis in GBM. RND1 directly interacted with p53, leading to the de-ubiquitination and reduced degradation of p53 protein. Further, it results in higher activity of p53-SLC7A11 signaling pathway, thus enhancing the ferroptosis of GBM. *P < 0.05; **P < 0.01; ***P < 0.001