Retinoids, Retinoic Acid Receptors, and Cancer
Abstract
Retinoids (i.e., vitamin A, all-trans retinoic acid, and related signaling molecules) induce the differentiation of various types of stem cells. Nuclear retinoic acid receptors mediate most but not all of the effects of retinoids. Retinoid signaling is often compromised early in carcinogenesis, which suggests that a reduction in retinoid signaling may be required for tumor development. Retinoids interact with other signaling pathways, including estrogen signaling in breast cancer. Retinoids are used to treat cancer, in part because of their ability to induce differentiation and arrest proliferation. Delivery of retinoids to patients is challenging because of the rapid metabolism of some retinoids and because epigenetic changes can render cells retinoid resistant. Successful cancer therapy with retinoids is likely to require combination therapy with drugs that regulate the epigenome, such as DNA methyltransferase and histone deacetylase inhibitors, as well as classical chemotherapeutic agents. Thus, retinoid research benefits both cancer prevention and cancer treatment.
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Retinoic acid can enhance or decrease expression of more than 500 genes depending on the target cell type and the physiological state of the organism.
“Retinoic acid can enhance or decrease expression of more than 500 genes depending on the target cell type and the physiological state of the organism [12,13].”
From Molecular Basis for Vitamin A Uptake and Storage in Vertebrates (2016) · cites this paper as [13]
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- Authors
- Tang, X.-H., & Gudas, L. J.
- Affiliations
- Weill Cornell Medicine (US)
- Venue
- Annual Review of Pathology: Mechanisms of Disease
- Publisher
- Annual Reviews
- Published
- 2011-02-28
- Volume
- 6
- Issue
- 1
- Pages
- 345-364
- ISSN
- 1553-4006 (ISSN-L)
- 1553-4014
- OpenAlex
- W2159159025
- Cited by
- 596
- References
- 7
- Citations by year
- 2026: 17 · 2025: 37 · 2024: 27 · 2023: 31 · 2022: 44 · 2021: 46 · 2020: 29 · 2019: 44 · 2018: 31 · 2017: 48 · 2016: 44 · 2015: 53 · 2014: 40 · 2013: 38 · 2012: 48
- FWCI
- 4.18
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annual Review of Pathology Mechanisms of Disease (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute for Health and Care Research
- National Institutes of Health
- National Cancer Institute (R01CA043796)
- National Institute of Dental and Craniofacial Research (R01DE010389)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Histone Deacetylase Inhibitors Research
- Keywords
- retinoids, retinoic acid receptor, vitamin A, all-trans retinoic acid, retinoid signaling, carcinogenesis, stem cell differentiation, breast cancer, estrogen signaling, retinoid resistance, epigenetic modifications, hypomethylating agents, histone deacetylase inhibitors, combination therapy, cancer prevention, cancer therapy
- MeSH terms
- Animals, Humans, Neoplasms, Retinoids, Signal Transduction, Receptors, Retinoic Acid
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