Fig. 1: Concomitant activation of IGF-IR/PI3K/AKT signaling and YAP1 in MLS tumor specimens and in vitro models. | Oncogenesis

Fig. 1: Concomitant activation of IGF-IR/PI3K/AKT signaling and YAP1 in MLS tumor specimens and in vitro models.

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

Fig. 1

A IHC stainings show strong expression of IGF-IR, IGF-II, and nuclear YAP1 in a representative MLS tissue specimen (original magnification, ×10; inset ×20). Venn diagram representing the overall concordance of IHC positivity (%). Bar chart summarizing overall IHC positivity of IGF-IR, IGF-II, and YAP1 of the MLS cohort (n = 54). B Immunoblots of SCP-1 mesenchymal stem cells transduced with FUS-DDIT3 or EV. C Effects of FUS-DDIT3 depletion on the IGF-IR/PI3K/AKT and Hippo/YAP1 pathways in MLS 1765-92 cells. D Subcellular fractionation of MLS 1765-92 cell lysates showing increased cytoplasmic p-YAP1 (Ser127) and diminished total YAP1 levels in the nuclear fraction upon RNAi-mediated silencing of FUS-DDIT3 for 72 h. GAPDH, cytoplasmic marker; Histone H3, nuclear marker. N nucleus, C cytoplasm. E Incubation of serum-starved MLS 1765-92 with recombinant IGF-II reverses the effects of FUS-DDIT3 depletion on p-LATS1 (Thr1079) and p-YAP1 (Ser127; Ser397). Representative immunoblots from at least three independent experiments are shown.

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