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. Author manuscript; available in PMC: 2016 Sep 22.
Published in final edited form as: Oncogene. 2015 Sep 21;35(22):2852–2861. doi: 10.1038/onc.2015.344

Figure 3.

Figure 3

The role of FGF2 and c-Fos in the regulation of anchorage-independent growth. (a) Representative photomicrographs and (b) quantification of soft agar colonies formed from DT12.4 cells cultured in the presence of tetracycline (−Fos) or absence of tetracycline (+Fos) showing increased colony number in c-Fos overexpressing cells with FGF2 treatment (10ng/ml). (c) Quantification of the number of FGF2-stimulated colonies in the absence or presence of c-Fos overexpression pre-treated with DMSO (control), or inhibitors of FGFR (20μM SU5402) or MEK (20μM PD98059) signalling. (d) Representative images and (e) quantification of anchorage-independent colonies from three c-Fos transgenic osteosarcoma cell lines, P1.15, P1.7, 131 P, in the absence and presence of FGF2 (10ng/ml). (f) Effects of FGF2 (10ng/ml) and SU5402 (SU; 20μM) on P1.7 cell number after monolayer culture, and (g) quantification of the number of soft agar colonies from P1.7 cells in the absence or presence of FGF2 (10ng/ml) or SU5402 (SU; 20μM) as indicated. (h) Dose-dependent inhibition of anchorage-independent colony growth of MG63 human osteosarcoma cells with the FGFR1 inhibitor, SU5402. The data represent the mean ± SD of triplicate samples. * p < 0.05 vs respective controls. Bars, a: 200μm; d: 400μm.