Figure 2 | Oncogene

Figure 2

From: Modulation of Wnt/β-catenin signaling and proliferation by a ferrous iron chelator with therapeutic efficacy in genetically engineered mouse models of cancer

Figure 2

HQBA rapidly inhibits expression of endogenous Wnt/β-catenin-response genes. (a) Endogenous Wnt/β-catenin target genes axin2 and cyclin D1 are inhibited by both β-catenin knockdown and HQBA. DLD-1 cells were treated with either small interfering RNA (siRNA) against β-catenin siRNA (72 h) or 4 μM HQBA (18 h) as indicated, and then target gene expression was quantitated by quantitative PCR. HQBA phenocopies the effect of β-catenin knockdown. *P<0.002; +P<0.015 for difference from control by two-tailed t-test. (b) The 18-h treatment of DLD-1 colon cancer cells with HQBA decreases levels of endogenous axin2 protein as determined by SDS–polyacrylamide gel electrophoresis and immunoblot. (c) DLD-1 cells were treated for 0–8 h with 4 μM HQBA, and abundance of the Wnt-responsive genes axin2 and c-Myc were measured by quantitative PCR. (d) HQBA suppresses expression of Wnt target gene Fgf8. Control midbrain to rhombomere 2 explants positive for the expression of Wnt1 (red) and Fgf8 (blue). (e) HQBA (1 μM) suppresses the expression of Fgf8 (blue). No change in the expression of Wnt1 was observed. (f) Ferrous ethylenediammonium sulfate (0.5 μM) was sufficient to rescue the expression of Fgf8 in the presence of 1.0 μM HQBA.

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