Fig. 5
CHD1L binds to HRE of HIF-2α targets to amply this crosstalk under hypoxia. A GO enrichment analysis revealed the related biological items based on CHD1L-related genes in the TCGA-KIRC cohort. B Heatmap showed the RT-qPCR results of HIF-2α targets in parental and CHD1L-KO 786-O cells. C Western blot assay showing the endogenous interactions between CHD1L and HIF-2α. D RT-qPCR assays reveal the mRNA levels of HIF-2α targets in control or CHD1L-KD cells under normoxia or hypoxia conditions. E RT-qPCR assays reveal the mRNA levels of CHD1L under normoxia or hypoxia. F RT-qPCR assays reveal the mRNA levels of HIF-1/2α in control or CHD1L-KO 786-O cells. G Parental and HIF-2α-KO 786-O cells were co-transfected with p2.1, PSV-Renilla, and a vector encoding FLAG-CHD1L or EV. Cells were exposed to 20% or 1% O2 for 24 h and subjected to dual-luciferase reporter assays (n = 3, mean ± SEM). H ChIP-qPCR assays showed the HIF-2α-binding to HREs of genes in parental and CHD1L-KO cells under normoxia or hypoxia for 12 h, individually. I RNA polymerase II ChIP-qPCR assays in parental and CHD1L-KO 786-O cells exposed to 20% or 1% O2 for 24 h (mean ± SEM, n = 3). J RT-qPCR assays showing the mRNA levels of HIF-2α targets of 786-O cells in the indicated groups under hypoxia for 12 h. K RT-qPCR assays showing the mRNA levels of HIF-2α targets of 786-O cells in the indicated groups under hypoxia for 12 h. *p < 0.05, **p < 0.01, ***p < 0.001, ns no significant