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. 2021 Oct 29;11:757678. doi: 10.3389/fonc.2021.757678

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Copyright © 2021 Ravegnini, De Leo, Coada, Gorini, de Biase, Ceccarelli, Dondi, Tesei, De Crescenzo, Santini, Corradini, Tallini, Hrelia, De Iaco, Angelini and Perrone

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Proposed mechanism of action of miR-499a-5p within the Wnt/β-catenin pathway. (A) The complex formed by AXIN, CK1α, GSK3β, and APC phosphorylates β-catenin, which subsequently undergoes the ubiquitin-proteasomal degradation. This prevents its nuclear translocation and pro-tumor gene transcription. (B) miR-499a-5p targets APC. High expression of miR-499a-5p promotes APC inhibition, thus preventing the AXIN/CK1α/GSK3β/APC complex formation. Without complex, β-catenin is not degraded, and it can translocate in the nucleus where it promotes gene transcription.