Fig. 6: DMF enhances sensitivity of ccRCC to sunitinib treatment.

A 786-O and RCC4 cells were individually divided into four groups, treated with vehicle, DMF, sunitinib, DMF plus sunitinib, respectively, then subjected to CCK-8 analysis to determine cell proliferation. B Colony formation assays and statistical analysis of the proliferation of 786-O and RCC4 cells treated with vehicle, DMF, sunitinib, DMF plus sunitinib, respectively. The data represent the mean ± SD of n = 3 independent experiments. Statistical differences were determined using ordinary one-way ANOVA. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, ns, not significant. C Schematic representation of the animal experiment. D 786-O cells were employed to mouse xenograft model and the mouse was administrated with DMF and/or sunitinib as indicated. Tumors were dissected from each group. E Tumor growth of each group was monitored. Statistical differences were determined using ordinary one-way ANOVA. ****P < 0.0001, ns, not significant. F The weight of tumors from each group was analyzed. Statistical differences were determined using ordinary one-way ANOVA. ***P < 0.001, ****P < 0.0001, ns, not significant. G IHC staining of HNF1B and Ki67 in xenograft tumors. H Quantifications of IHC images. Statistical differences were determined using ordinary one-way ANOVA. ****P < 0.0001, ns, not significant. I Working model depicting the mechanism of DMF-mediated HNF1B degradation and ccRCC inhibition.