Research Paper Volume 11, Issue 23 pp 10839—10860
HIF-2α upregulation mediated by hypoxia promotes NAFLD-HCC progression by activating lipid synthesis via the PI3K-AKT-mTOR pathway
Figure 1. HIF-2α was upregulated in NAFLD-HCC patients and correlated with poor survival. (A, B) Quantitative RT-PCR assessment of HIF-1α and HIF-2α expression in tissues from NAFLD-HCC patients (n=7) and other HCC patients (n=21). Transcription levels were normalized to those of β-actin. (C). Western blot analysis of HIF-2α expression in the patients’ tissues. β-Actin was used as the loading control. Densitometric analyses of the band intensity ratios for HIF-2α/β-actin. (D) IHC determination of HIF-2α expression in tissues from HCC and NAFLD-HCC patients (magnification: 200X, 400X). H score between NAFLD-HCC and HCC (E, F) Survival curves of 139 patients with HCC and NAFLD-HCC. (G, H) Survival curves of 139 patients stratified according to HIF-2α protein expression.