Abstract
AXIN proteins are major components of the β-catenin destruction complex or degradasome, which limits β-catenin nuclear translocation and Wnt signalling activation at steady state. Schmidt etal. performed quantitative analysis of cellular AXIN protein levels in human colorectal cancer cells and revealed that AXIN2 plays a non-redundant role in regulating the total AXIN pool and Wnt/β-catenin signalling activity. Tankyrase (TNKS) inhibitors failed to inhibit Wnt/β-catenin signalling in AXIN2 knockout cells, suggesting that AXIN2 is essential for TNKS inhibitors to function. Mechanistically, the authors show that AXIN2 recruits TNKS to AXIN1 and promotes TNKS-mediated degradation of AXIN1. These findings may have important implications for anti-cancer therapy by TNKS small molecule inhibitors.
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