Fig. 7: GR promotes cisplatin-resistant cell survival and tumor growth via MAST1-MEK-ERK.

a, b Effect of MAST1 overexpression on cell viability and MEK/ERK activity in GR attenuated KB-3-1 and A2780 cells with cisplatin treatment. GR was target downregulated by GR shRNA (a) or mifepristone (10 μM) (b). MEK and ERK activity was assessed by S221 MEK and T202/Y204 ERK phosphorylation. c–e Effect of MAST1 overexpression on tumor growth of xenograft mice bearing GR knockdown KB-3-1 cells. Mice were treated with cisplatin (2 mg/kg i.p. twice/week) from 4 days after xenograft. Tumor volume (c), tumor weight and Ki-67 staining (d), and phosphorylation of MEK and ERK in tumors (e) are shown. f, g Effect of MAST1 knockdown on cell viability and MEK/ERK activity in GR enhanced KB-3-1 and A2780 cells with cisplatin treatment. GR was enhanced by GR overexpression (f) or dexamethasone (500 nM) (g). h–j Effect of MAST1 knockdown on tumor growth of xenograft mice bearing GR overexpressed KB-3-1 cells. Mice were treated with cisplatin (4 mg/kg i.p. twice/week) from 4 days after xenograft. Tumor volume (h), tumor weight and Ki-67 IHC staining (i), and MEK and ERK activity in tumors (j) are shown. Scale bars represent 5 mm for (c, h), and 50 μm for (d, i). Data are from three independent biological experiments for (a, b, f, g) and n = 8 mice/group for c–e and h–j. One representative data are shown for (right panels of d and i; e and j). Data are mean ± SD for (a, b, d, f, g, i) and mean ± SEM for c and h. Statistical analyses were performed by two-way ANOVA for c and h, and one-way ANOVA for others. Source data are provided as a Source Data file.