Fig. 5From: Pharmacological targeting of the ephrin receptor kinase signalling by GLPG1790 in vitro and in vivo reverts oncophenotype, induces myogenic differentiation and radiosensitizes embryonal rhabdomyosarcoma cellsGLPG1790 triggers myogenic differentiation and counteracts ERMS stem-like phenotype. a Cell lysates from RD and TE671 cells untreated (DMSO) (−) or treated (+) with GLPG1790 for indicated times were analysed by immunoblotting with specific antibodies for indicated proteins; α-Tubulin expression shows the loading of samples. Representative of three independent experiments. b Immunofluorescence experiments showing the expression of MYOD1 and MyHC, at 72 h after GLPG1790 treatment. Images captured under ApoTome microscope at 40× magnification. c Representative microphotographs of RD and TE671 cells in adherent conditions (Adherent) and in stem cell (SC) medium after 15 days of incubation in the absence (SC-DMSO) or in the presence of 3.5 μM GLPG1790 (SC-GLPG1790). d Histograms of percentage of CD133 positive cells determined by FACS analysis. Results represent the mean values ± SD of four independent experiments. Statistical significance: **p < 0.01, ***p < 0.001 vs. Adherent, $$$ p < 0.001 vs. SC-DMSO. e Histograms of percentage of CXCR4 positive cells determined by FACS analysis. Results represent the mean value of four independent experiments ± SD. Statistical significance: **p < 0.01, ***p < 0.001 vs. Adherent, $$ p < 0.01 vs. SC-DMSO. f Western blot analysis of Nanog in protein lysates from RD and TE671 cells in adherent, SC-DMSO or SC-GLPG1790 cultured conditions for 15 days; α-Tubulin expression shows equal loading of samples. Representative of three independent experimentsBack to article page