Skip to main content
. Author manuscript; available in PMC: 2018 Apr 28.
Published in final edited form as: Oncogene. 2016 Nov 28;36(17):2423–2434. doi: 10.1038/onc.2016.395

Figure 1.

Figure 1

KDM1A expression was reduced in differentiated GSCs. (a) GSC10 were subjected to immunofluorescence staining to detect the presence of the stemness markers CD133 and nestin. (b) GSCs were isolated from patient-derived GBM using established stem cell marker CD133 and differentiation was induced in the presence of 10% FBS for 7 days. KDM1A expression was examined in stem and differentiated GSCs using Western blotting. (c) GSCs (GSC10, GSC11 and U251-GSCs) were isolated from patient-derived GBM (GBM10, GBM11) and U251-GBM cells, respectively, and treated with KDM1A inhibitors NCL-1 and NCD-38 for 7 days, and the number of neurospheres were counted. (d) Undifferentiated and differentiated GSCs were treated with vehicle, NCL-1 or NCD-38 for 72 h, and the cell viability rates were measured by CellTiter-Glo assays. All the results were representative of three independent experiments. (e) Replicate cultures of GSC10 were treated with vehicle, NCL-1 or NCD-38 for 48 h followed by Annexin V-FITC and propidium iodide (PI) staining for 15 min. The Annexin V–positive apoptotic populations were determined by using flow cytometry. Data are represented as mean ± s.e. *P < 0.05, **P < 0.01, ***P < 0.001 based on the Student’s t-test.