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. Author manuscript; available in PMC: 2016 Apr 21.
Published in final edited form as: Cell Rep. 2015 Apr 9;11(3):446–459. doi: 10.1016/j.celrep.2015.03.040

Figure 5. L2185A mutation confers resistance to mTOR kinase inhibitors in colorectal cancer models.

Figure 5

(A) SW480 cells carrying homozygous WT mTOR or L2185A mutant alleles were treated with various concentrations of AZD8055, INK-128, OSI-027 and PP242 for 2 day. Growth of SW480 cells was measured by SRB assay. Data represent means ± SD in three independent experiments.

(B) SW480 cells carrying homozygous WT and L2185A mutant mTOR allele were treated with a single dose of AZD8055 (100 nM), INK-128 (100nM), OSI-027 (6,000 nM), and PP242 (2,000 nM) for different times. Cell growth was measured by SRB assay. The drug carrier DMSO was used as a control. Data represent means ± SD in three independent experiments.

(C) SW480 cells carrying homozygous WT and L2185A mutant mTOR were treated with various concentrations of INK-128, OSI-027, AZD8055 and PP242 for 1 hr. The effect on the level of P-S6K, S6K, P-4E-BP1, 4EB-P1, P-AKT and AKT was analyzed by immunoblot.

(D) SW480 cells carrying homozygous WT and L2185A mutant mTOR alleles were treated with various concentrations of BEZ235, PF-0691502 and Torin2 for 2 day. The growth of SW480 cells was measured by SRB assay. Data represent means ± SD in three independent experiments.