Fig. 2
CHD1L enhances RCC malignant progression in vitro and in vivo. A Colony formation and Transwell (right) assays of CHD1L-KD 786-O cells with or without WT CHD1L restoration. The western blot assay showing CHD1L proteins was exhibited on the left side. B Quantification of colony or migration numbers in the indicated groups. C Soft agar colony formation showed the numbers in control or CHD1L-deficient 786-O cells. D Sphere formation assay revealed the stemness features of parental or CHD1L-deficient 786-O cells. E Measurement of subcutaneous tumor growth of control and CHD1L-deficient 786-O cells (2-way ANOVA followed by Tukey’s multiple comparisons tests), scale bar = 1 cm. F Kaplan–Meier analysis was used to compare the survival differences in the indicated groups. G Representative bioluminescence graphs showed the metastatic signals in mice injected with control or CHD1L-KO 786-O cells, individually. H Generation of RCC patient-derived organoids (PDOs) and representative growth images in the PDOs transfected with shCtrl or shCHD1L lentiviruses. Quantification of PDO diameters in the indicated groups. Scale bar = 100 μm. I CCK-8 assays showed the cell growth rates in HIF-2α−/low RCC cells transfected with shCtrl or shCHD1L lentiviruses. J Representative graphs of HIF2high and HIF2low/− ccRCC PDOs treated with shCtrl or shCHD1L#1 viruses for 10 days. Scale bar = 100 μm. *p < 0.05, **p < 0.01, ***p < 0.001, ns no significant