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. 2023 Mar 3;14:1124111. doi: 10.3389/fendo.2023.1124111

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Copyright © 2023 Souza, Macheroni, Pereira, Vicente and Porto

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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Illustration of the molecular regulatory mechanisms responsible for the expression of the non-phosphorylated β-catenin and Galectin-3 induced by estrogen receptor activation. Activation of estrogen receptors ESR1 and ESR2 by E2, PPT or DPN increases (arrows) the phosphorylation of SRC, ERK1/2 or AKT and the expression of non-phosphorylated β-catenin, Cyclin D2, VEGF and Galectin-3, which in turn can modulate nuclear transcriptional events, such as, proliferation, migration, invasion, and anchorage-independent growth of androgen-independent prostate cancer cells PC-3 (A) and DU-145 (B) (see 54, 67, 68, 73–76 for more information). TF (transcription factor).