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. 2023 Apr 6;11(4):1105. doi: 10.3390/biomedicines11041105

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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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Antitumor mechanism of intermittent administration of high-dose androgens in CRPC cells. Development of castrate-resistant tumor cells involves acquisition of adaptive auto-regulation giving place to an increase in AR expression in a low androgen environment. This increase inhibits apoptotic death and stimulate cancer cell proliferation. AR is needed for DNA replication in CRPC cells. When these cells are acutely exposed to supraphysiologic androgen, AR is saturated. This induces a paradoxical cancer cell death via over-stabilizing AR, preventing full relicensing in the next cell cycle.