RICTOR overexpression contributes to melanoma-targeted therapy resistance through STAT pathway (A) The expression of RICTOR, phosphorylated AKT and ERK, total AKT and ERK, phosphorylated STAT3 (Y705), and total STAT3 were assessed by Western blotting in the A375 melanoma cell line and two independent clones of A375 Vemurafenib resistant to vemurafenib (A375R1 and A375R2). (B,C) A375 parental and resistant cell lines cells were seeded at low density and treated three times a week with inhibitors or DMSO, Vemurafenib (10 μM), OSI-027 (3 μM), or the combination of both for 10 days. Graphs represent the mean ± s.d. of an experiment in triplicate (similar results were obtained in three independent experiments). (D) A375 parental and resistant cell lines cells were treated for 24 h with DMSO, Vemurafenib (10 μM), or OSI-027 (3 μM), and the expressions of RICTOR, phosphorylated AKT and ERK, total AKT and ERK, phosphorylated STAT3 (Y705), and total STAT3 were assessed by Western blotting.