Phosphorylation-Dependent Regulation of WNT/Beta-Catenin Signaling

Frontiers in Oncology

Kinjal Shah²  Julhash U. Kazi² 

[1] Division of Translational Cancer Research, Department of Laboratory Medicine, Lund University, Lund, Sweden;Lund Stem Cell Center, Department of Laboratory Medicine, Lund University, Lund, Sweden;

关键词: β-catenin;    CTNNB1;    GSK3β;    adherens junctions;    AXIN;    CK1;   

DOI  :  10.3389/fonc.2022.858782

来源: DOAJ

【 摘 要 】

WNT/β-catenin signaling is a highly complex pathway that plays diverse roles in various cellular processes. While WNT ligands usually signal through their dedicated Frizzled receptors, the decision to signal in a β-catenin-dependent or -independent manner rests upon the type of co-receptors used. Canonical WNT signaling is β-catenin-dependent, whereas non-canonical WNT signaling is β-catenin-independent according to the classical definition. This still holds true, albeit with some added complexity, as both the pathways seem to cross-talk with intertwined networks that involve the use of different ligands, receptors, and co-receptors. β-catenin can be directly phosphorylated by various kinases governing its participation in either canonical or non-canonical pathways. Moreover, the co-activators that associate with β-catenin determine the output of the pathway in terms of induction of genes promoting proliferation or differentiation. In this review, we provide an overview of how protein phosphorylation controls WNT/β-catenin signaling, particularly in human cancer.

【 授权许可】

Unknown