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. 2017 Dec 17;9(4):4496–4510. doi: 10.18632/oncotarget.23388

Figure 4. Oncogenic RAS/BRAF/MEK pathway activates Shh signaling.

Figure 4

(A) HEK293T cells were transfected with Gli-Luc reporter (pGL3-Gli-Luc) together with BRAF V600E, HRAS G12V and MEK S218E/S222E active forms and luciferase activity was measured 48 hours after transfection. Gli1 transfection was used as positive control. (B, C). Inhibition of MEK impaired Gli luc activation. 8505C cells were transfected with Gli-Luc reporter (pGL3-Gli-Luc). After 24 hours cells were treated with U0126 at 10 μM for 6 and 24 hours and Shh activation was evaluated by Luciferase assay (B) and Q-RT-PCR to test Gli1 relative expression (C). Error bars represent standard deviations of experimental triplicates. **p = ≤ 0.01; *p = ≤ 0.05.