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. 2009 Dec 15;102(2):351–360. doi: 10.1038/sj.bjc.6605486

Figure 2.

Figure 2

Hypoxia inducible factor (HIF)-1α and HIF-2α accumulated in breast cancer cells with hypoxia and they potentiated Notch signaling. (A) Western blot analysis of HIF-1α (the upper band marked by the arrow) and HIF-2α expression in breast cancer cells under 21% O2 or 1% O2 culture conditions for 24 h. H, hypoxia; N, normoxia. (B) Enhanced ICN3 signaling by HIF-1α or HIF-2α as determined by an in vitro Notch reporter assay, which was inhibited by dominant negative MAML1. (C) Hypoxia inducible factor (HIF)-1α and HIF-2α synergise with MAML1 in potentiating ICN3-mediated Notch signaling. (D) Enrichment of HIF-1α at HES1 promoter by hypoxia in MCF7 cells. Fold enrichment of the binding of HIF-1α to the RBP-Jκ binding sites of human HES1 promoter in MCF7 cells under 1% O2 culture condition. Normal IgG or HIF-1α-specific antibodies were used for CHIP experiments followed by real-time PCR with primers flanking the RBP-Jκ binding sites of HES1 promoter. H, hypoxia; N, normoxia; *P<0.01. (E) Increased binding of NOTCH3 intracellular domain to the RBP-Jκ binding sites of HES1 promoter in MCF7 cells under hypoxia. H: hypoxia; N, normoxia; *P<0.05.