A. In canonical pathway, binding of a Wnt ligand to a frizzled receptor triggers a signaling cascade contributes to betacatenin translocation to the nucleus. Beta-catenin binds to the T-cell factor/lymphoid enhancer factors (TCF/LEFs) transcription factors mediating the upregulation of Wnt target genes. In the absence of Wnt ligands, cytoplasmic beta-catenin molecules bind to a destruction complex which phosphorylates and targets β-catenin for proteasomal degradation. B. In noncanonical Wnt/planar cell polarity (PCP) pathway, the binding of Wnt ligands to frizzled receptors activates Rho and Rac small GTPases leading to the cytoskeletal changes and gene transcription. In Wnt/Ca2+ pathway, PLC (phospholipase C) activation leading to the release of intracellular Ca ++ , then activates Ca ++ dependent signaling pathways like CaN (calcineurin) /NFAT (nuclear factor of activated T cells) (Figure was constructed using Biorender (https://biorender.com)).

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... processes of tumorigenesis, including tumor initiation, tumor growth, cell senescence, cell death, differentiation and metastasis. On the other hand, the noncanonical Wnt pathways (including the wnt/Ca2+, wnt/planar cell polarity) are activated independent of β-catenin and have been implicated in both oncogenic or tumor suppressor functions (33) (Fig. 5A ,B). (Figure was constructed using Biorender ...