Fig. 2: LOXL1 promotes gliomagenesis and enhances IR resistance.

a,b U87 cells stably expressing luciferase were engineered to overexpress LOXL1 or Vec as a control. These cells (2 × 10⁵ per mouse) were intracranially injected into athymic nude mice. Bioluminescence imaging of tumor growth was conducted (a, left panel). Real-time images are presented, and the luciferase intensities were quantified (a, right panel). After 35 days, the tumors were removed from the mouse brains and examined. Representative images of hematoxylin and eosin (H&E)-stained coronal brain sections from tumor xenografts are shown. Scale bar, 100 μm (b). Representative images of tumor boundaries are presented. The data are presented as the mean luciferase intensities ± SD of 4 mice per group. ***p < 0.001. c, d LN18 cells stably expressing luciferase were transfected with shLOXL1 to knock down LOXL1 or shNT as a control. The processes of bioluminescence imaging and H&E staining are described in Fig. 2a, b. n = 4. e, f GSC11 cells stably expressing luciferase were transfected with shLOXL1 to knock down LOXL1 or shNT as a control. The processes of bioluminescence imaging and H&E staining are described in Fig. 2a, b. g Survival durations of mice injected with glioma cells (log-rank test). h-j Cells were intracranially injected into randomly selected athymic nude mice (four mice per group). After the U87-Vec and U87-LOXL1 groups reached appropriate tumor sizes, the mice were treated with or without IR (γ) radiation (4 Gy) and continually maintained for 3 days. Bioluminescence imaging of tumor growth was conducted. Real-time images are presented (h, left panel), and the luciferase intensities were quantified (h, right panel). The data are presented as the mean luciferase intensities ± SD of 4 mice per group. Survival durations of these implanted mice were compared (i). Furthermore, a TUNEL assay was performed to determine the number of apoptotic cells in the tumors following exposure to IR (j). ***p < 0.001. n.s., not significant.