Encyclopedia of Cancer

Living Edition
| Editors: Manfred Schwab

Retinoic Acid and Cancer

  • Noa NoyEmail author
  • Joseph L. Napoli
Living reference work entry

Latest version View entry history

DOI: https://doi.org/10.1007/978-3-642-27841-9_5071-4


All- trans-retinoic acid (atRA, Fig. 1), a pale yellow lipid-soluble compound, serves as an activated metabolite of vitamin A (retinol) that is required for embryonic development and normal function of postnatal tissues. atRA acts through genomic and nongenomic mechanisms, by controlling transcription and translation. atRA activates nuclear receptors, thereby regulating expression of more than 500 target genes. atRA activates the retinoic acid receptors RARα, RARβ, and RARϒ, as well as the peroxisome proliferator-activated receptor β/δ (PPARβ/δ). In addition, the 9- cis-RA (9cRA) isomer (Fig. 1) also is transcriptionally active. In vitro, 9cRA activates both RAR and the retinoid X receptors, RXRα, RXRβ, and RXRϒ. 9cRA occurs in pancreas β cells, in which it reduces glucose-stimulated insulin secretion, but it remains uncertain whether it occurs in other tissues that express RXR – thus, its physiological significance remains incompletely understood. Synthetic compounds that...
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  1. Levi L, Wang Z, Doud MK, Hazen SL, Noy N (2015) Saturated fatty acids regulate retinoic acid signalling and suppress tumorigenesis by targeting fatty acid-binding protein 5. Nat Commun 23(6):8794–8804. PMCID: 4662070CrossRefGoogle Scholar
  2. Napoli JL (2005) Vitamin A, β-carotene and cancer. Chapter 3. In: Awad AB, Bradford PG (eds) Nutrition and cancer prevention. CRC Press, Boca Raton, pp 61–74Google Scholar
  3. Napoli JL (2012) Physiological insights into all-trans-retinoic acid biosynthesis. Biochim Biophys Acta 1821(1):152–167. PMCID: 3179567CrossRefPubMedGoogle Scholar
  4. Napoli JL (2017) Cellular retinoid binding-proteins, CRBP, CRABP, FABP5: effects on retinoid metabolism, function and related diseases. Pharmacol Ther 173:19–33. PMCID: 5408321CrossRefPubMedGoogle Scholar
  5. Noy N (2010) Between death and survival: retinoic acid in regulation of apoptosis. Annu Rev Nutr 21(30):201–217CrossRefGoogle Scholar
  6. Noy N (2016) Non-classical transcriptional activity of retinoic acid. Subcell Biochem 81:179–199CrossRefPubMedGoogle Scholar
  7. Soprano DR, Qin P, Soprano KJ (2004) Retinoic acid receptors and cancers. Annu Rev Nutr 24:201–221CrossRefPubMedGoogle Scholar
  8. Stevison F, Jing J, Tripathy S, Isoherranen N (2015) Role of retinoic acid-metabolizing cytochrome P450s, CYP26, in inflammation and cancer. Adv Pharmacol 74:373–412CrossRefPubMedPubMedCentralGoogle Scholar
  9. Tang XH, Gudas LJ (2011) Retinoids, retinoic acid receptors and cancer. Annu Rev Pathol 6:345–364CrossRefPubMedGoogle Scholar
  10. Uray IP, Dmitrovsky E, Brown PH (2016) Retinoids and rexinoids in cancer prevention: from laboratory to clinic. Semin Oncol 43:49–64CrossRefPubMedGoogle Scholar

See Also

  1. Iskakova M, Karbyshev M, Piskunov A, Rochette-Egly C (2015) Nuclear and extranuclear effects of vitamin A. Can J Physiol Pharmacol 93(12):1065–1075CrossRefPubMedGoogle Scholar
  2. Retinol. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 3292. doi: https://doi.org/10.1007/978-3-642-16483-5_5076
  3. Vitamin A. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 3925. doi: https://doi.org/10.1007/978-3-642-16483-5_6205
  4. Vitamin D receptor. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 3928. doi: https://doi.org/10.1007/978-3-642-16483-5_6208
  5. Wei LN (2016) Cellular retinoic acid binding proteins: genomic and non-genomic functions and their regulation. Subcell Biochem 81:163–178CrossRefPubMedGoogle Scholar

Copyright information

© Springer-Verlag GmbH Germany 2018

Authors and Affiliations

  1. 1.Department of Cellular and Molecular Medicine, Lerner Research InstituteCleveland Clinic and Case Western Reserve UniversityClevelandUSA
  2. 2.Program in Metabolic Biology, Nutritional Sciences and ToxicologyUniversity of CaliforniaBerkeleyUSA