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Editorial: Targeting the Wnt/β-catenin signaling pathway in cancer, volume II

Sep 2026 · Frontiers in Oncology · Vol 16 · 0 citations
Medicine

TL;DR

Together, these studies emphasize that Wnt/ b -catenin signaling is controlled at multiple regulatory levels and cellular compartments, supporting context-speci c and biomarker-guided therapeutic strategies.

Abstract

this Research Topic. In lung adenocarcinoma (LUAD), miR-582-3p promotes Wnt/ b -catenin pathway activation through suppression of PTPRCAP, whereas WTAP-mediated m6A modi fi cation decreases SOX2 mRNA stability and limits SOX2-dependent Wnt/ b -catenin signaling. In triple-negative breast cancer (TNBC), SOX10 acts as an upstream transcriptional regulator associated with Wnt/ b -catenin activation and malignant phenotypes. In colorectal cancer (CRC), PTHrP promotes Ser552 phosphorylation and nuclear accumulation of b -catenin and is associated with reduced oxaliplatin sensitivity, including effects mediated by the tumor microenvironment. LGR5 represents a Wnt-responsive cancer stem-cell marker and R-spondin receptor that links pathway ampli fi cation with stemness, in fl ammation, tumor microenvironment interactions, and therapeutic resistance. Finally, emerging b -catenin-directed approaches, including PROTACs and other precision degraders, aim to preferentially eliminate oncogenic cytoplasmic and nuclear b -catenin while preserving the cadherin-associated membrane pool required for cell-cell adhesion. Together, these studies emphasize that Wnt/ b -catenin signaling is controlled at multiple regulatory levels and cellular compartments, supporting context-speci fi c and biomarker-guided therapeutic strategies. APC, adenomatous polyposis coli; CK1, casein kinase 1; CRC, colorectal cancer; EMT, epithelial-to-mesenchymal

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