Fig. 2: HIF-1α regulates and promotes NAT10 transcription in ccRCC.

a The effect of HIF-1α-specific small interfering RNA on mRNA knockdown in 786-O cells by qRT-PCR. b Western blot analysis of HIF-1α protein knockdown in 786-O cells.c The level of NAT10 mRNA in 786-O cells was also decreased after HIF-1α knockdown by qRT-PCR. d Western blot analysis showed that the level of NAT10 protein decreased after HIF-1α knockdown in 786-O cells. e Dual luciferase reported that HIF-1α was overexpressed, the relative activity of firefly luciferase fused with the wild-type or NAT10 promoter (0, +300) mutant plasmid in 786-O cells. f ChIP-qPCR showed that HIF-1α can bind to the NAT10 promoter region (0, +300), VEGFA was the positive control and β-actin was the negative control. g Left: Representative images of in situ HIF-1α expression levels in 25 pairs of ccRCC cancer tissues and adjacent tissues detected by immunohistochemical staining. Scale: 100μm (left); 50 μm (right). Statistical analysis of the intensity of immunohistochemical staining (right). h Kaplan–Meier analysis survival for ccRCC patients based on HIF-1α expression (p = 0.0468, log-rank test).