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. Author manuscript; available in PMC: 2015 Jul 3.
Published in final edited form as: Cell. 2014 Jun 19;158(1):171–184. doi: 10.1016/j.cell.2014.06.004

Figure 2. YAP1 rescues KRAS mutant cancer cells in vitro.

Figure 2

(A) Morphology of HCTtetK cells expressing the indicated vectors at 20x magnification. The indicated ORFs were expressed and cells were treated with doxycycline (KRAS suppressed). (B) Viability of HCTtetK cells upon KRAS suppression in cells expressing the indicated genes, normalized to cell viability in media condition. (C) Consequences of expressing YAP1 in KRAS-mutant cell lines after KRAS suppression. Viability of shKRAS normalized to shLuciferase in the presence of each indicated ORF. (D) Response of HCT116 cells to MYC suppression in cells that express the indicated ORFs. (E) Effect of YAP1 suppression on anchorage independent growth of HA1E transformed with KRASG13D or YAP1 ORF. (F) Effect of doxycycline-induced KRAS suppression on activation of ERK, AKT, and S6 in HCTtetK cells expressing LacZ, KRAS, or YAP1. (G) Effect of a PI3K inhibitor (PI3Ki; GDC-0941) or a MEK inhibitor (MEKi; AZD-6244) on the ability of YAP1 to rescue KRAS suppression. Cells were treated with 1uM of GDC-0941, 1uM of AZD-6244, both, or DMSO. Data normalized to viability of cells without KRAS suppression (media) with DMSO treatment. (B–E, G) Mean ± SD of at least 3 replicates in a representative experiment shown. See also Figure S2.