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. 2023 Feb 16;15(6):1325–1350. doi: 10.1016/j.jcmgh.2023.02.004

Figure 2.

Figure 2

PFKFB4 expression was extrinsically driven by hypoxia in HCC. (A) RNA-seq analysis for PFKFB4 expression in a panel of 4 HCC cell lines under normoxic and hypoxic conditions. (B) qPCR analysis for PFKFB4 and HIF-1α expression in Huh7 and MHCC97L cells at the indicated time points under hypoxic treatment. (C) Western blot analysis for PFKFB4 and HIF-1α expression in Huh7 and MHCC97L cells at the indicated time points under hypoxic treatment. (D) qPCR and Western blot analysis for PFKFB4 expression in MHCC97L cells with stable HIF-1α and HIF-2 knockdown under normoxic and hypoxic conditions. (E) ChIP-qPCR assay showed the positive interactions between the HIF-1α and the 2 HREs at -166 and -402 upstream positions of the PFKFB4 promoter in Huh7 and PLC/PRF/5 cells under hypoxia. (F) A schematic illustrating the overall in silico data integration strategy for the identification of functionally significant hypoxia-inducible genes in HCC. NT, Non-tumor; shHIF, shRNA against hypoxic-inducible factor; shNTC, non-targeting control shRNA; T, Tumor.