Fig. 2

Aberrant Wnt/β-catenin signaling pathway activation in tumor. Genetic abnormalities and epigenetic modifications can activate the Wnt/β-catenin pathway, leading to the onset of tumorigenesis. Mutations of tumor suppressor genes decrease the activity of the destruction complex, contributing to tumor growth. RNF43 loss-of-function mutations that increase Wnt receptor abundance on the cell surface, rendering tumors sensitive to Wnt inhibitors and decreasing negative feedback at the receptor-level to drive tumor growth. Loss of DNA methylation results in aberrant transcription of target genes, including WIF1, SFRP, DKK1, DACT, SOX7/17, β-TrCP, E-Cadherin, APC, AXIN-2, Wnt7a/9A. Histone modifications, such as methylation, acetylation, and phosphorylation, regulate the Wnt/β-catenin signaling pathway in tumors by controlling chromatin accessibility and gene expression of Wnt pathway components and downstream targets, impacting tumor initiation, progression, and metastasis. Non-coding RNA, including lncRNA and miRNA, modulate the Wnt/β-catenin signaling pathway in tumors by targeting key components such as β-catenin, Wnt ligands, receptors, and genes