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. 2018 Sep 24;9(10):988. doi: 10.1038/s41419-018-1015-x

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — a Western blot analyses of the GSC markers (CD133, SOX2, and OLIG2) and VDAC2 in GSCs expressing VDAC2 or control vector. b In vitro limiting dilution assay of the self-renewal capacity of GSCs expressing VDAC2 or control vector. Ectopic expression of VDAC2 decreases GSC self-renewal capacity (***p < 0.001). c, d Representative bioluminescent images (c) and the quantification (d) of xenografts derived from GSCs expressing VDAC2 or control vector at day 10 and day 20 after tumor cell implantation. VDAC2 overexpression markedly suppresses GSC-driven tumor formation. p photons, sr steradian (***p < 0.001). e Kaplan–Meier survival analysis of mice bearing xenografts derived from GSCs expressing VDAC2 or control vector. n = 5/group. f, g Quantification of the level of VDAC2 (f) or GSC marker SOX2 (g) in GBM xenografts derived from GSCs expressing VDAC2 or control vector through IHC staining (***p < 0.001)