Fig. 2: IGF-IR/PI3K/AKT-mediated regulation of YAP1 in MLS. | Oncogenesis

Fig. 2: IGF-IR/PI3K/AKT-mediated regulation of YAP1 in MLS.

From: Fusion protein-driven IGF-IR/PI3K/AKT signals deregulate Hippo pathway promoting oncogenic cooperation of YAP1 and FUS-DDIT3 in myxoid liposarcoma

Fig. 2

A IGF-II stimulation of starved MLS 402-91 and MLS 1765-92 cells activates the IGF-IR/PI3K/AKT cascade, associated with reduced p-LATS1 (Thr1079), p-YAP1 (Ser127), and p-YAP1 (Ser397) protein levels. Treatment with BMS-754807 (IGF-IR inhibitor) or LY294002 (PI3K inhibitor) for 30 min shows inverse effects. B IGF-II stimulation of starved MLS 402-91 and MLS 1765-92 cells for 6 h significantly increases TEAD luciferase reporter activity (error bars represent the mean + SD of three independent experiments; unpaired t test, ***P < 0.001). C, D Treatment with BMS-754807 or LY294002 leads to a dose-dependent reduction of TEAD luciferase reporter activity (error bars represent the mean + SD of three independent experiments, unpaired t test; *P < 0.05, **P < 0.01, ***P < 0.001); ns, not significant. E, F Decreased YAP1 levels upon RNAi-mediated silencing of IGF-IR or PIK3CA for 72 h compared to non-targeting control siRNA. Representative immunoblots of at least three independent experiments with similar results are shown.

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