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. 2023 Jan 20;24(3):2046. doi: 10.3390/ijms24032046

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© 2023 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Crosstalk between PI3K/AKT/mTOR and AR signaling pathways. The two signaling pathways are closely connected and regulated according to a reciprocal feedback mechanism. AR inhibition reduces FKBP5 levels, inhibiting PHLPP-mediated suppression of AKT, thereby activating AKT. Activation of AKT then generates upregulation of AR by several mechanisms, including direct phosphorylation of AR and nuclear exclusion of FOXO1. AKT: protein kinase B; AR: androgen receptor; ARE: androgen response element; FKBP5: FK506 binding protein 5; FOXO1: forkhead box transcription factor 1; GPCR: G-protein coupled receptor; mTOR: mammalian target of rapamycin; PIP3: phosphatidylinositol-3,4,5-triphosphate; PHLPP: PH domain of leucine repeat sequence-rich phosphatase; PSA: prostate-specific antigen; PTEN: phosphatase and tensin homolog; RTK: receptor tyrosine kinase.