Fig. 5

X-ray irradiation promotes the SP1-mediated transcription of PRDM10-DT in a ROS-dependent manner. A ROS levels in X-ray- or C-ion-irradiated A549 and H1299 cells. n = 3. B The potential transcription factors capable of binding to the PRDM10-DT-promoter region were predicted via the UCSC, hTFtarget, and AnimalTFDBv4.0 databases, and intersections were made with all existing human (Homoall) transcription factors. The binding scores of 21 filtered TFs in the PRDM10-DT-promoter region were predicted via the JASPAR database. C The top 10 TFs in B were silenced in X-ray-irradiated A549 cells via siRNA, and the PRDM10-DT transcriptional level was subsequently measured. n = 3. D A luciferase reporter vector containing the PRDM10-DT promoter region sequence and plasmids containing RREB1, YY1, and SP1 wild-type (wt) or mutant (mut) sequences were cotransfected into A549 cells, which were subsequently subjected to 2 Gy X-ray or 200 μM H₂O₂ treatment, and the luciferase activity was measured after treatment. n = 3. E A ChIP experiment was carried out to detect the connection of SP1 in the PRDM10-DT promoter region with or without ROS. n = 3. F After si-SP1 transfection or 200 nM mithramycin treatment, A549 and H1299 cells were exposed to 2 Gy X-rays. Next, the relative transcript expression levels of VEGF, TGF-β1, PRDM10-DT, and SP1 were determined. n = 3. G The levels of the SP1, TGF-β1, and VEGF proteins in cells subjected to various treatments. n = 3. H Schematic diagram illustrating X-ray-induced PRDM10-DT transcriptional activation and the downregulation of angiogenesis induced by ROS deletion or pharmacological inhibition of SP1. The data are presented as the means ± standard deviations (SDs). * p < 0.05; ** p < 0.01; and *** p < 0.001