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. 2021 Jul 9;13(14):3452. doi: 10.3390/cancers13143452

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© 2021 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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Androgen deprivation therapy (ADT) modulates epidermal growth factor receptor (EGFR) signaling and activates epithelial-to-mesenchymal transition (EMT) to escape from ADT. ADT modulates EGFR signaling and initiates EMT via four mediators: androgen receptor (AR) variants AR8, fucosyltransferase 8 (FUT8), AR overexpression, and phosphatidylinositol-4-phosphate 5-kinase type 1 alpha (PIP5K1A)/Akt signaling. Stimulated EGFR activate β-catenin and Ras signaling, which augments the expression of EMT-related transcription factor TWIST1 and others. A black arrow represents signal transduction; a red arrow represents cell fate; an orange arrow represents stimulations from ADT.