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. 2011 May;31(10):2053–2065. doi: 10.1128/MCB.01094-10

Fig. 5.

Fig. 5.

Positive role of axin during Wnt signaling in colon cancer cells. TopFlash assays in HCT116 and SW480 colon cancer cells (A) or HEK293T and RKO cells treated with control, β-catenin, or AXIN siRNAs (B) were performed. In panel A, AXIN1 and AXIN2 siRNAs inhibit the constitutive Wnt pathway activation due to mutations in APC (SW480) or β-catenin (HCT116), while in panel B AXIN1 plus AXIN2 knockdowns potentiate the Wnt3A-stimulated activity of the reporter. (C) Activation of the Wnt pathway in HEK293T cells using a degradation resistant β-catenin mutant (pt.β-catenin) is inhibited by AXIN1 plus AXIN2 siRNAs. Figures are representative of at least three independent experiments performed in duplicates, where the error bars represent the standard errors. In panel A, TopFlash levels are expressed as the percent activation compared to the basal constitutive levels observed with control siRNA (100%).