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. Author manuscript; available in PMC: 2016 Sep 1.
Published in final edited form as: Cancer Res. 2015 Jun 30;75(17):3623–3635. doi: 10.1158/0008-5472.CAN-14-2999-T

Figure 4. RAS/MAPK signaling confers resistance to Smo inhibitor.

Figure 4

(A–C) Relative survival for SMB21 cells expressing candidate genes treated with LDE225 (72 hrs). HRAS(G12V), BRAF(V600E), not PIK3CA(H1047R) or myristoylated AKT, confer resistance. (mean ± s.e.m., n > 5).

(A’) Elevated phospho-Erk in SMB21 cells expressing HRAS(G12V) or BRAF(V600E).

(B’–C’) Elevated phospho-AKT in SMB21 cells expressing PIK3CA(H1047R) or AKT(Myr).

(D) SMB21(HRAS) cells initiate resistant tumors in vivo. Tumor volume over time. Mean ± s.e.m., n = 5. (Experiments were performed concurrently with Fig. 2C, the same SMB21 control shown here and Fig 2C.)

(E) Phospho-Erk in sensitive and resistant tumors from engrafted SMB21 cells mean ± s.e.m, * p < 0.05, unpaired student t-test.