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. 2016 Dec 30;8(10):16728–16743. doi: 10.18632/oncotarget.14377

Figure 5. The compounds induces Fli-1 transcriptional activity through MAPK/ERK.

Figure 5

A. Indicated compounds induce phosphorylation of MAPK/ERK in CB7 cells. B. Induction of MAPK/ERK by A236 can be blocked by the MEK inhibitor U0126 (U). Phosphorylation was not blocked by JNK SP600125 (Sp) or P38 SB203580 (Sb) inhibitors, respectively, but partially by the RAF inhibitor Sorafenib tosylate (St). C. A75- and TPA-induced phosphorylation of MAPK/ERK is inhibited by U0126 in HEL cells. D. Induction of MAPK/ERK phosphorylation by A75 and TPA is blocked by addition of both U0126 and BCR-ABL inhibitor Imatinib in K562 cells, E. Fli-1 transcriptional activity induced by the indicated compounds in HEK293T cells co-transfected with FB-Luc+MigR1-Fli-1 is blocked by MEK inhibitor U0126. F. Western blot analysis for Fli-1 expression in CB7 and HEL cells after treatment with A75, A89 and A228. Compound concentration in experiments A-F, 2μM. Concentration of MAPK/ERK inhibitors, 5μM.