Figure 7. Mechanism of the regulation of Wnt-β-catenin signaling by hsa-miR-150-5p. In the presence of Wnt ligands and Wnt agonists such as R-Spondin (R-Spo), cytoplasmic disheveled (Dvl) is recruited to the membrane receptors, resulting in subsequent phosphorylation and activation of low-density lipoprotein receptor-related protein 5/6 (LRP5/6). These events lead to the titration of the active destruction complex composed of glycogen synthase kinase 3 (GSK3β), casein kinase I (CK1), adenomatosis polyposis coli (APC), and Axin. As a consequence, β-catenin is stabilized and accumulated in the cytoplasm, resulting in the nuclear translocalization of β-catenin, where it activates Wnt signaling through its interaction with the TCF/LEF (T-cell factor/lymphoid-enhancing factor) nuclear complex [57, 58]. Hsa-miR-150-5p prevents the activation of Wnt signaling (red lines) by reducing the expression levels of its targets: (i) β-catenin-Wnt signaling activator (Figure 1B, Figure 2, Figure 3, Figure 5, and Figure 6), (ii) the AKT3 enhancer of β-catenin stabilization through inhibition of GSK3β (Figure 1B, Figure 2, Figure 3, and Figure 5), and (iii) the JARID2 activator of Wnt signaling through the repression of Wnt antagonist-secreted frizzled-related protein 1 (SFRP1; Figure 1B, Figure 2, Figure 3, and Figure 5). This results in a decreased expression level of the Wnt target gene AXIN2 and an increased expression level of TCF3, a Wnt signaling transcriptional repressor.