Corresponding Author: Yunhui Liu

Department of Neurosurgery, Shengjing Hospital of China Medical University, No. 36, Sanhao Road, Heping District, Shenyang 110004 (China)


In the article “Roundabout4 Suppresses Glioma-Induced Endothelial Cell Proliferation, Migration and Tube Formation in Vitro by Inhibiting VEGR2-Mediated PI3K/AKT and FAK Signaling Pathways” [Cell Physiol Biochem 2015;35:1689-1705. DOI: 10.1159/000373982] by Cai et al., a number of incorrect panels were included in Figure 4C and Figure 8C during Figure assembly. Specifically, Control and Robo4(-) representative images in endothelial cell medium group and Control, Robo4(-) NC representative images in glioma conditioned medium group of Figure 4C were incorrect in the original article. Control, Robo4(-)NC, Robo4(-), Robo4(-)+LY294002 representative image of Figure 8C was incorrect in the original article.
In preparation of a previous Erratum the authors state that they did not review all the original images, only those about which concerns were raised. They state that they have now reviewed all the original data and state that all the original data in this paper are authentic and all the statistical results and conclusions are correct. The authors submitted the entire original data to the journal and this submitted data reflects that presented in the figures.
The authors have requested to correct Figure 4C and Figure 8C, due to an error caused by incorrect assembly of representative pictures in the process of panel incorporation.

The corrected Figure 4 and Figure 8 are shown here.

Fig. 4. Effect of Robo4 on glioma-induced endothelial cell proliferation, migration, and tube formation in vitro. Endothelial Cell viability was measured by CCK-8 proliferation assay, and results were expressed as percent viability, from left to right, the lanes are in control, Robo4(+) NC, Robo4(+), Robo4(-) NC and Robo4(-), respectively. Migration of endothelial cell was measured by transwell migration assay, and results were expressed as the number of migrated cells per field (magnification, ×200; scale bar, 100µm). Tube formation of ECs was measured, and results were expressed as relative tubule length and number of branches (magnification, ×100; scale bar, 100µm). Data represent means ± SD (n = 5, each). *P<0.05 vs. Robo (+) NC group, #P<0.05 vs. Robo (-) NC group.

Fig. 8. VEGR2 mediate PI3K/AKT and FAK signaling pathways were involved in the Robo4-regulated glioma angiogenesis in vitro. After ECs in glioma conditioned medium were pretreated with VEGFR2 inhibitor SU-1498(10uM), AKT inhibitor LY294002(10uM) and FAK inhibitor 14(5uM) for 24 hours, ECs proliferation (A), migration (B) and Tube formation (C) are showed. Data represent mean ± SD (n = 5, each). *P<0.05 vs. Robo4 (-) NC group, #P<0.05 vs. Robo4 (-) group.