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. Author manuscript; available in PMC: 2013 May 1.
Published in final edited form as: Nat Commun. 2012;3:1168. doi: 10.1038/ncomms2173

Figure 6. Sos-mediated cross activation of WT Ras by oncogenic K-Ras is required for tumor growth.

Figure 6

(a) MIA PaCa-2 cells harboring the indicated inducible constructs were injected subcutenously into mice. Following injections, animals were fed doxycyline-containing diet and tumor growth was measured as described in Methods. Values are means +/- SD from three independent experiments. (b) Representative mice and tumors are shown. (c) Signaling analysis of the indicated xenografts. ERK activity was assessed by immunoblotting for pERK and K-Ras-GTP levels were determined by RBD pull down. Tubulin was used as a loading control. (d) Values of ERK activity are presented as fold activation compared to shCtrl and represent means +/- SD from three independent experiments. (e) Cell proliferation of the indicated xenografts as assessed by immunohistochemical staining for Ki-67. Images shown are representative of three independent experiments. Scale bars, 50 μm. (f) Schematic depiction of the role of Sos in oncogenic Ras-driven tumorigenesis. The binding of oncogenic Ras (Onc.) to the allosteric site promotes the activation of WT Ras. The signaling output of both forms of Ras is required for tumorigenesis.