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. Author manuscript; available in PMC: 2020 Feb 5.
Published in final edited form as: Cancer Res. 2018 Mar 23;78(11):2886–2896. doi: 10.1158/0008-5472.CAN-17-3386

Figure 1: Sunitinib resistance is associated with increased AR expression, and AR inhibition restores drug sensitivity in RCC models.

Figure 1:

(A) RPPA data indicate increased AR expression in RP-R-01 RCC PDX model at the time of resistance. (B) Immunohistochemistry and (C) qRT-PCR analysis indicating AR expression in RCC PDX models sensitive (ss) and resistant (sr) to sunitinib. (D-F) mRNA, Western blot analysis and proliferation assay on RCC cell lines, indicate increased AR expression in tumor cells that are less sensitive to sunitinib. IC50 for sunitinib correlates with AR status. (G) Cell viability assay of RCC cell lines treated with either sunitinib, enzalutamide or combination, for 48hrs indicates synergistic decrease in cell viability in the combination group, only in the presence of AR expression. (H) Ki67 immunofluorescence staining and quantitation of 786-0R cells treated with either sunitinib, enzalutamide or combination. (I) Proliferation assay with different sunitinib concentrations shows the shift in IC50 between AR expressing 786-0 cell (786-0AR), compared to parental cell line. Bar graphs represent the mean ± SD. *p<0.05, **p<0.0016, ***p<0.0009, ****p<0.0001, ns= not significant.