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. 2013 Jan 28;110(7):2569–2574. doi: 10.1073/pnas.1216462110

Fig. 3.

Fig. 3.

PI3K activated by different growth factors or constitutive mutation causes YAP nuclear accumulation. (A) Similar to EGF treatment (Fig. 1), LPA treatment or serum treatment induced YAP nuclear accumulation through PI3K-PDK1 pathway in confluent serum-starved MCF-10A cells, independent of EGFR activity. Cells in c–f received a 30-min inhibitor treatment, followed by a 30-min LPA treatment. a, no treatment; b, LPA treatment only; c, Wortmannin; d, PDK1 inhibitor II; e, BX795; f, Iressa. Cells in h–k received a 30-min inhibitor treatment, followed by a 30-min serum treatment. g, serum treatment only; h, Wortmannin; i, PDK1 inhibitor II; j, BX795; k, Iressa. YAP intracellular localization was determined by confocal microscopy. (Scale bar: 20 μm.) (B) Inhibition of PI3K or PDK1 activity blocks YAP nuclear accumulation caused by PIK3CA constitutive mutation in MCF-7 cells. Serum-starved MCF-7 cells were treated with PI3K inhibitor (Wortmannin) or PDK1 inhibitor (BX795) for 4 h, after which YAP intracellular localization was determined by confocal microscopy. (Scale bar: 20 μm.)