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. 2018 Nov 5;12(12):2191–2208. doi: 10.1002/1878-0261.12395

Figure 3.

Figure 3

AXL‐mediated epirubicin resistance depends on c‐MYC activity. (A) FLO‐1 cells were treated with vehicle, epirubicin (1 μm) alone, epirubicin (1 μm) in combination with 10058‐F4 (5 μm), or 10058‐F4 (5 μm) alone for 24 h. Cell viability was evaluated by MTT assay. (B) To measure the c‐MYC transcriptional activity, FLO‐1 cells were transfected with 4xEMS‐Luc reporter and β‐galactosidase plasmids, and treated with vehicle or 10058‐F4 (5 μm) for 24 h. (C) Western blot analysis of caspase‐3 and PARP proteins in FLO‐1 cells after treatment with vehicle, epirubicin alone, epirubicin in combination with 10058‐F4, or 10058‐F4 alone as described in panel A. (D) FLO‐1 cells were subjected to Knockdown of c‐MYC by shRNA or control shRNA and treated with vehicle or epirubicin (1 μm) for 24 h. Cell viability was assessed by MTT assay. (E) FLO‐1 cells with control or c‐MYC knockdown and treated with vehicle or epirubicin, as described in panel D, were subjected to western blot analysis of caspase‐3 and PARP proteins. Gel loading was normalized for equal β‐actin. Data from three independent experiments are represented as mean ± SEM. Statistical significance was evaluated by Student's t‐test.