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. 2024 Nov 19;6(1):vdae187. doi: 10.1093/noajnl/vdae187

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© The Author(s) 2024. Published by Oxford University Press, the Society for Neuro-Oncology and the European Association of Neuro-Oncology.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.

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Figure 3. — SKF96365 and DPI-201-106 induce cell cycle arrest in glioblastoma patient-derived cell lines. GBM6, GBM39, and SB2 cells were treated with 10 µM of SKF96365 (A-C) or DPI-201-106 (D-F), and the cell cycle was analyzed after 3 days. Data shown are mean ± SD and statistical significance was determined with a 2-way ANOVA and Šidák’s multiple comparison test. Apoptosis was determined after treatment with 10 µM SKF96365 or DPI-201-106 after 3 and 7 days in (G) GBM, (H) GBM39, or (I) SB2. Data shown are mean ± SD, and statistical significance was determined with a 2-ANOVA and Dunnett’s multiple comparison test. p21 and p27 expression was determined after 24, 48, and 72 h after treatment with 10 µM SKF96365 or DPI-201-106 in (J) GBM6, (K) GBM39, or (L) SB2 cells. The cell cycle was synchronized with a double thymidine block in SKF96365 or DPI-201-106-treated (M) GBM6, (N) GBM39, and (O) SB2 cells to analyze mitotic markers. Asynchronized cells (Asy) are shown as controls. *P < .05, **P < .01, ***P < .001, ****P < .0001.