Fig. 3.

PRMT2 is required for the maintenance of GSCs and tumorigenesis. a Representative images of tumor spheres in dose of 10 cells/well are shown. Scale bar, 200 µm. b, c In vitro limiting dilution assays plating decreasing number of GSCs with or without PRMT2 knockdown calculated with extreme limiting dilution assay analysis in U87 and T98G cells (b), and TPC1115 and TPC0411 cells (c) (mean ± SD, n = 3). Frequency and probability estimates were computed using the ELDA software. ***p ≤ 0.001. d Representative luciferase images of three mice per group at 7, 14, and 28 days post tumor implantation. U87 or TPC1115-luciferase cells were transduced with shScr or shPRMT2. Color scale for U87 cells: Min = 5.00 × e⁶, Max = 5.00 × e⁸ (top panel); color scale for TPC1115 cells: Min = 5.00 × e⁴, Max = 2.00 × e⁵ (bottom panel). e The average signals of luciferase activity in implanted mice brains at different time points were respectively compared in U87 and TPC1115 cells transduced with shScr or shPRMT2 (mean ± SD; n = 6). Significance level was determined using Student’s two-sided t-tests. ***p ≤ 0.001. f Survival analysis of mice intracranially implanted with U87 cells with or without PRMT2 knockdown. X axis represents days after cells injection. Significance level was determined using log-rank analysis. *p ≤ 0.05, **p ≤ 0.01. n = 6 for each treatment group. g Representative images of H&E staining for tumor formation in control (shScr) and PRMT2-depletion group (shPRMT2). Top panel: scale bar, 2 mm. Bottom panel: scale bar, 200 µm