Fig. 2: Endocan is essential for establishing the hypervascular phenotype of GBM.

a Images of the brains collected from 7080 glioma-bearing Esm1 WT or Esm1 KO mice (upper panel). H&E staining of the tumor slices (middle panel, Scale bar, 200 μm) and CD31 staining of the tumor slices (lower panel, Scale bar, 200 μm). b Quantitation of the diameter of the blood vessels formed in tumors from PTEN/P53/NF1 deleted glioblastoma model. CD31 positive VE cells were imaged and then measured using ImageJ vessel analysis tool. n = 7 regions from n = 5 mice were used for the analysis, ****P < 0.0001, unpaired two-tailed Student’s t test. c Representative transmission electron microscopy images of tumors formed in Esm1 WT and KO mice (middle panel) and contralateral tissue region from non-tumor hemisphere (lower panel). Green and magenta lines indicate the outer and inner diameter of the blood vessels respectively. Scale bar, 2 µm. d Violin plots show frequency of blood vessel ratio of Shape Adjusted Eclipse (SAE) distributions (y-axis). Center lines denote median values obtained by the SAE approach after determining vessel area or perimeter of blood vessels in the tumor-bearing hemisphere of mice brains and contralateral region. **P = 0.0030, One-way ANOVA followed by post hoc test. e Proliferation of rEndocan treated (10 ng/ml) and untreated TEC cells (TEC 15 and TEC 14). Proliferation was measured on Day 5 post-treatment, n = 4 biological replicates, **P = 0.0012 for TEC15 and ***P = 0.0013 for TEC14, unpaired two-tailed Student’s t test. f Proliferation of TEC15 and TEC14 cells treated with conditioned media collected from the control GBM cells or GBM cells pretreated with rEndocan (10 ng/ml) for 3 days. Proliferation was measured on day 5 post-treatment, n = 3 biological replicates, *P = 0.0173 for TEC15 and ***P = 0.0002 for TEC15, unpaired two-tailed Student’s t test. Source data are available in the Source Data file.