PLK1 stabilizes β-catenin to drive colorectal carcinogenesis through NFKB2-mediated transcriptional activation of USP2a and site-specific phosphorylation

Theranostics 2026 Open access

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Authors: Yan Michael Li, Lili Zhao, Jiaqiang Deng, Songmei Lu, Jingyu Du, Chen Chen, Li Zhao, Zhiyun Xu, Wencan Wang, Yundi Wang, Fangdong Zou
DOI: 10.7150/thno.122368
Cited by: 1

Abstract

Our study identified PLK1 as a key regulator of β-catenin signaling flexibility in CRC, coordinating kinase-dependent and transcriptional mechanisms to sustain pathway activation. The discovery of the PLK1-NFKB2-USP2a-β-catenin axis provides a novel therapeutic rationale for targeting PLK1 to selectively disrupt Wnt-driven tumorigenesis, potentially overcoming the toxicity limitations of conventional Wnt inhibitors.

Fields of Study & Subjects

Microtubule and mitosis dynamics Wnt/β-catenin signaling in development and cancer Ubiquitin and proteasome pathways

Publication details

Journal / source
Theranostics
Publisher
Ivyspring International Publisher
Volume
16
Issue
7
Pages
3488–3506
Publication date
1 January 2026
Language
EN