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Hepatocellular carcinoma-linked mutations drive low Wnt/β-catenin activity enabling niche-independent growth and YAP/TAZ signaling.

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iScience 📖 저널 OA 100% 2023: 4/4 OA 2024: 21/21 OA 2025: 69/69 OA 2026: 112/112 OA 2023~2026 2026 Vol.29(1) p. 114501
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Venhuizen AJ, van Os Y, Kaptein ML, Aarts MT, Xanthakis D, Jordens I, Maurice MM

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AXIN1 organizes assembly of a destruction complex that degrades the transcriptional co-activator β-catenin, thereby preventing inappropriate Wnt/β-catenin signaling.

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APA Venhuizen AJ, van Os Y, et al. (2026). Hepatocellular carcinoma-linked mutations drive low Wnt/β-catenin activity enabling niche-independent growth and YAP/TAZ signaling.. iScience, 29(1), 114501. https://doi.org/10.1016/j.isci.2025.114501
MLA Venhuizen AJ, et al.. "Hepatocellular carcinoma-linked mutations drive low Wnt/β-catenin activity enabling niche-independent growth and YAP/TAZ signaling.." iScience, vol. 29, no. 1, 2026, pp. 114501.
PMID 41550750 ↗

Abstract

AXIN1 organizes assembly of a destruction complex that degrades the transcriptional co-activator β-catenin, thereby preventing inappropriate Wnt/β-catenin signaling. In hepatocellular carcinoma (HCC), mutations associate with a poor-prognosis subtype distinct from β-catenin-mutant HCC (). To assess how -deficiency drives HCC, we introduced HCC-associated and mutations in human liver cancer cells and liver-derived organoids. We show that mutations activate Wnt/β-catenin signaling to varying but generally lower levels than mutations. Strikingly, premature 5'-end stop codons do not yield knockout mutations but drive alternative translation of N-terminally truncated AXIN1 variants with partial suppressor activity. All variants enable liver progenitor organoids to grow without Wnt and R-spondin, indicating downstream Wnt/β-catenin activation. Additionally, Wnt/β-catenin signaling inversely correlates with YAP/TAZ-mediated signaling, leaving higher YAP/TAZ activity in -mutant versus -mutant cells. Thus, mutations drive physiologically relevant Wnt/β-catenin activation, providing a permissive environment for YAP/TAZ signaling, thereby distinguishing them from mutations.

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