Fig 1: POS attenuates CSCs stemness in GBM cells. (A) Self-renewal capacity was detected by a sphere formation assay after the cells were treated as indicated for 2 weeks. Scale bar, 50 µM. (B) Expression levels of the CSCs marker proteins CD133, SOX2, Nanog and Oct4 were measured by western blotting after the cells were treated as indicated for 24 h. (C) CD44+/CD133+ subpopulations were monitored by flow cytometry after the cells were handled as in (B).
Fig 2: POS impairs CSCs stemness via inducing autophagy in GBM cells. (A) Self-renewal capacity was detected by a sphere formation assay after the cells were treated with or without POS in the presence or absence of CQ for 2 weeks. Scale bar, 50 µM. (B) Expression levels of the CSCs marker proteins CD133, SOX2, Nanog and Oct4 were measured by western blotting after the cells were treated with or without POS in the presence or absence of CQ for 24 h. (C) Efficacy of Atg5 shRNA was validated by western blotting. (D) Expression levels of the CSCs marker proteins CD133, SOX2, Nanog and Oct4 were examined by western blotting after the Atg5 shRNA or shNC cells were treated with or without POS for 24 h.
Fig 3: POS decreases GBM tumor growth in vivo. (A) U87-MG cells were subcutaneously implanted into immunodeficient nude mice. The mice were randomly divided into 2 groups and administered DMSO or POS at intervals of 3 days for a total of 6 administrations. The tumor volumes were detected every 3 days. Left, tumor images were photographed on the 18th day. Right, tumor volumes was measured at different time points (n = 5). (B) Expression of LC3, CD133, survivin and β-catenin in U87-MG xenografts that were collected from DMSO or POS-treated mice was measured by immunohistochemical analysis. Scale bar: 40 μM.
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