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. 2015 Nov 13;7(1):610–621. doi: 10.18632/oncotarget.6311

Figure 5. Compound 968 reverses acquired erlotinib resistance by blocking GAC activity in HCC827ER cells.

Figure 5

(A) HCC827 cells were cultured in RPMI 1640 supplemented with 10% FBS, and were treated with compound 968 at 0, 1, 5, and 10 μM concentrations for 48 hours (left panel) or treated with 10 μM compound 968 for 0, 12, 24 and 48 hours (right panel). The EGFR and GAC expressions were determined by Western blot. (B) HCC827ER cells were cultured in RPMI 1640 supplemented with 10% FBS, and were treated with compound 968 at 0, 1, 5, and 10 μM concentrations for 48 hours (left panel) or treated with 10 μM compound 968 for 0, 12, 24 and 48 hours (right panel). The EGFR and GAC expressions were deterimine by Western blot. (C) HCC827 (left panel) and HCC827ER (right panel) cells were cultured in RPMI 1640 supplemented with 10% FBS, and were treated with compound 968 (10 μM), or erlotinib (1 μM), or compound 968 (10 μM) combined with erlotinib (1 μM) for 48 hours respectively. The EGFR and GAC expressions were determined by Western blot. (D) HCC827 and HCC827ER cells were cultured in RPMI 1640 supplemented with 10% FBS, and were treated with compound 968 (10 μM), or erlotinib (1 μM), or compound 968 (10 μM) combined with erlotinib (1 μM) for 48 hours respectively, then mitochondria was isolated from different cells, and GAC activity was determined by glutaminase activity assay. Data represent the average of three independent experiments (mean ± SD). **P < 0.01, ***P < 0.001.