Fig. 6
CHD1L enhances colony formation, migration, and stemness of RCC cells depending on HIF-2α. A CCK-8 assays showing the cell growth rates in parental and HIF-2α-KO (HKO) 786-O cells expressing EV or CHDL1 exposed to 20% or 1% O2 for 12 h. B–D Colony formation, migration, or stemness abilities were detected in cells in the indicated groups. E A subcutaneous tumor model was generated by the indicated cells and the tumor growth curve was shown. F Tumor weight was calculated and compared with tumors from the indicated groups. G Co-IP assays were used to confirm the endogenous interactions between CHDL1 and BRD4. H HIF luciferase reporter assays in 786-O cells transfected with indicated plasmids and exposed to 20% or 1% O2 for 24 h in the presence of doxycycline. The FLuc/RLuc activity was determined (mean ± SEM, n = 3). I BRD4 ChIP-qPCR assays in parental and CHD1L-KO 786-O cells exposed to 20% or 1% O2 for 12 h (mean ± SEM, n = 3). J Colony formation assays were conducted in cells treated with increasing doses of JQ1. K A subcutaneous tumor model was generated to confirm the in vivo response of RCC cells to JQ1. L MTT analysis of CHD1L-KD 786-O and OSRC-2 cells underwent JQ1 treatment with increasing doses (0, 3 μM, or 6 μM). M Illustration of CHD1L-hijacked loop with BRD4/HIF-2α. *p < 0.05, **p < 0.01, ***p < 0.001, ns no significant