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. 2019 Jul 9;9(16):4795–4810. doi: 10.7150/thno.30988

Figure 8.

Figure 8

HIF-1α is reciprocally regulated by FOXC2 in transcriptional level (A) Schematic illustration of FOXC2 binding site on the HIF-1α promoter region. (B, C) RNA and protein levels of HIF-1α were measured in hypoxic PANC-1/BxPC-3 cells treated with siFOXC2 or FOXC2-OE. (D) ChIP assessments of PANC-1/BxPC-3 cells with anti-FOXC2 antibody. qRT-PCR of ChIP assay showing the accumulation of HIF-1α promoter bound to the FOXC2. (E) PANC-1 cells underwent transfection using MUT or WT plasmid as reporter cells. The luciferase activity was measured and normalized. (F, G) HIF-1α levels were detected hypoxic PANC-1/BxPC-3 cells following siCF129 and CF129-OE transfection. (H) ChIP assessment of PANC-1 cells transfected using vector or plasmid targeting CF129 via anti-FOXC2 antibody. (I) PANC-1 cells transfected using WT or MUT plasmid as reporter cells, were transfected with vector or CF129-OE. Luciferase activity was measured and normalized. (J) Protein levels of HIF-1α were assessed in PANC-1 cells treated using CF129-OE or/and FOXC2-OE during hypoxia. (K) Protein levels of HIF-1α were detected in PANC-1 cells treated with siFOXC2 or/and siCF129 during hypoxia. (L) The graphical representation of the reciprocal feedback of CF129-mediated HIF-1α and FOXC2 in pancreatic cancer. * P< 0.05,**P<0.01.