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Fig. 4 | Journal of Hematology & Oncology

Fig. 4

From: Pharmacological targeting of the ephrin receptor kinase signalling by GLPG1790 in vitro and in vivo reverts oncophenotype, induces myogenic differentiation and radiosensitizes embryonal rhabdomyosarcoma cells

Fig. 4

GLPG1790 decreases wound closure and anchorage-dependent or -independent clonogenic ability of ERMS cells. RD and TE671 cells untreated (DMSO) or treated with GLPG1790 were seeded at low concentration in a anchorage-dependent conditions or b anchorage-independent conditions. Colonies were photographed and counted after 8 days of treatment. Results represent the mean values ± SD of three independent experiments. Statistical significance: *p < 0.05 and ***p < 0.001 compared with the respective control (DMSO), arbitrarily set at 1. c Wound healing experiments in RD and TE671 cells. A scratch was made at time 0 and maintained for 24 h in the presence of GLPG1790 or DMSO. The dotted lines represent the edges of the wound. Photographs were taken under light microscope (10x magnification). The migration index was plotted in bar graphs. Statistical significance: **p < 0.01 compared with the respective control (DMSO), arbitrarily set at 1. d Cell lysates from RD and TE671 cells treated with or without GLPG1790 for the indicated hours were analysed by immunoblotting with specific antibodies against integrin αV, integrin β1, integrin β3 and integrin β5; α-Tubulin expression shows the loading of samples. Representative of three independent experiments

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