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. 2022 Oct 20;23(20):12622. doi: 10.3390/ijms232012622

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© 2022 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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Molecular mechanisms of retinoid action in keratinocyte carcinomas. BCC (left) and cSCC (right). Retinoids have been shown to (1) downregulate PI3K signaling, (2) promote apoptosis through regulation of the extrinsic death receptor pathway and mitochondrial cell death pathway (3) suppression of Gli transcription to limit PTCH1 pathway activation as well as increase in Tig3 tumor suppressor transcription. In cSCC, (4) spectral properties of retinoids protect against UV damage (5) decrease Ap-1 activation (6) promote proapoptotic (Fas, Faslg, Tig3, Casp8) and tumor suppressor (Rarb) gene expression (7) inhibit oncogenic STAT3 activation (8) downregulate Ras-Raf-MEK-ERK signaling. Figure created using Biorender.com.