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Figure 2
Figure 2.The hypoxic microenvironment induces lipid accumulation in HCC and steatotic HCC cells by upregulating HIF-2α. (A, B) Quantitative RT-PCR assessment of HIF-2α expression in HCC and steatotic HCC cells under hypoxic conditions. Transcription levels were normalized to those of β-actin. (C) Western blot analysis of HIF-2α expression in HCC and steatotic HCC cells under hypoxic conditions. β-Actin was used as the loading control. (D) Densitometric analyses of the band intensity ratios for HIF-2α/β-actin. (E) Oil red O staining and quantification in HCC and steatotic HCC cells with or without hypoxia treatment. (F, G) Triglyceride levels in HCC and steatotic HCC cells subjected to different durations of hypoxia.
Figure 2 — HIF-2α upregulation mediated by hypoxia promotes NAFLD-HCC progression by activating lipid synthesis via the PI3K-AKT-mTOR pathway | Aging