Fig. 2: CK1δ promotes tumor progression through stabilizing NRAS mutants.
From: Pharmacological targeting of casein kinase 1δ suppresses oncogenic NRAS-driven melanoma
a SK-MEL-103 cells were transfected with empty vector or FLAG-NRAS Q61R and treated with DMSO or PF670462 (5 µM) for 24 h. Western blotting was performed with indicated antibodies. b Cell proliferation assay was performed from cells in (a). c The migration and invasion abilities of cells as in (a) were measured by Transwell migration and invasion assays. d Cells as in (a) were treated with DMSO or indicated concentrations of dacarbazine (DTIC) and cell survival was determined. e SK-MEL-103 cells stably expressing shScramble (shScr) or shCK1δ were transfected with empty vector or indicated plasmids. Western blotting was performed with indicated antibodies. f Cell proliferation of cells in (e) was examined. g Cells as in (e) were treated with indicated concentrations of DTIC and cell survival was determined. The results represent mean ± s.d. from three independent experiments. h, i Cells as in (a) were subcutaneously implanted into nude mice (5–6 weeks, n = 6). When tumors reached around 150–200 mm3 in size, mice were treated with saline, PF670462 (4 mg/kg), dacarbazine (8 mg/kg) or PF670462 plus dacarbazine. Tumors were collected (h) and weights were measured (i). The results represent the mean ± s.d. of data from six mice. Data were presented as mean ± SD of three independent experiments (b–d, f, g). Data were analyzed by two-sided one-way ANOVA in (b, c, f, i). Source data are provided as a Source Data file.
