Fig. 7
Targeting CHD1L renders HIF-2αhigh RCC sensitive to sunitinib treatment. A Dose–response curves and IC50 of cells treated with CHD1Li. Data are presented as mean ± SD (n = 6) from one-of-three independent experiments. B CCK-8 assays showing the efficacy of CHD1Li in suppressing HIF-2αhigh or HIF-2αlow/− RCC. C Dose–response curves and IC50 of CHD1L-KO or OE cells treated with sunitinib. D CCK-8 assays were used to detect growth rates of cells treated with DMSO, sunitinib, CHD1Li, or Comb. E Colony formation assays showed the colony numbers of cells treated with indicated drugs. F Immunohistochemistry (IHC) images showed the CHD1Lhigh or CHD1Llow RCC-PDXs (left). The subcutaneous tumor model was shown on the right to exhibit tumors from the indicated groups (right). G Quantification of the tumor growth curve of tumors from the indicated groups. H Representative BLI of orthotopic RCC tumors formed by CMV-Luc 786-O cells in BALB/c nude mice after daily oral gavage with Vehicle control, sunitinib (15 mg/kg), CHD1Li (20 mg/kg), or Comb once daily (n = 8 mice per group). Right: Dynamic measurements of BLI in treated tumors over time. I Quantification of BLI signals of mice from the indicated groups. J Kaplan–Meier survival curve analysis showed the differential survival outcomes in mice from indicated groups. *p < 0.05, **p < 0.01, ***p < 0.001, ns no significant