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Cited by 403Retinoids in leukemia and cellular processesPeroxisome Proliferator-Activated ReceptorsPsoriasis: Treatment and Pathogenesis

The DOI matches its Crossref record; 1,341 of the 1,341 references it cites were found in a registry or an index.

Retinoic acid receptors: From molecular mechanisms to cancer therapy

di Masi, Alessandra, Leboffe, Loris, De Marinis, Elisabetta, Pagano, Francesca, Cicconi, Laura, Rochette-Egly, Cécile, Lo-Coco, Francesco, Ascenzi, Paolo, Nervi, Clara·2015·Molecular Aspects of Medicine
DOI 10.1016/j.mam.2014.12.003
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Abstract

Retinoic acid (RA), the major bioactive metabolite of retinol or vitamin A, induces a spectrum of pleiotropic effects in cell growth and differentiation that are relevant for embryonic development and adult physiology. The RA activity is mediated primarily by members of the retinoic acid receptor (RAR) subfamily, namely RARα, RARβ and RARγ, which belong to the nuclear receptor (NR) superfamily of transcription factors. RARs form heterodimers with members of the retinoid X receptor (RXR) subfamily and act as ligand-regulated transcription factors through binding specific RA response elements (RAREs) located in target genes promoters. RARs also have non-genomic effects and activate kinase signaling pathways, which fine-tune the transcription of the RA target genes. The disruption of RA signaling pathways is thought to underlie the etiology of a number of hematological and non-hematological malignancies, including leukemias, skin cancer, head/neck cancer, lung cancer, breast cancer, ovarian cancer, prostate cancer, renal cell carcinoma, pancreatic cancer, liver cancer, glioblastoma and neuroblastoma. Of note, RA and its derivatives (retinoids) are employed as potential chemotherapeutic or chemopreventive agents because of their differentiation, anti-proliferative, pro-apoptotic, and anti-oxidant effects. In humans, retinoids reverse premalignant epithelial lesions, induce the differentiation of myeloid normal and leukemic cells, and prevent lung, liver, and breast cancer. Here, we provide an overview of the biochemical and molecular mechanisms that regulate the RA and retinoid signaling pathways. Moreover, mechanisms through which deregulation of RA signaling pathways ultimately impact on cancer are examined. Finally, the therapeutic effects of retinoids are reported.

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Research works printed but not linked: 11

  1. Delescluse, 1991, Selective high affinity retinoic acid receptor α or β-γ ligands, Mol. Pharmacol, 40, 556
  2. Fukutani, 1995, Isoforms of PML-retinoic acid receptor alpha fused transcripts affect neither clinical features of acute promyelocytic leukemia nor prognosis after treatment with all-trans retinoic acid, Leukemia, 9, 1478
  3. Funk, 1912, The etiology of the deficiency diseases, Beri-beri, polyneuritis in birds, epidemic dropsy, scurvy, experimental scurvy in animals, infantile scurvy, ship beri-beri, pellagra, J.State Med, XX, 341
  4. Grimwade, 2000, Blood, 96, 1297
  5. Maignan, 1987, Bicyclic naphthalenic derivatives, a process for their preparation and their use in pharmaceuticals and cosmetics, Eur. Pat. Appl, 220, 118
  6. Mandelli, 1997, Molecular remission in PML/RARα-positive acute promyelocytic leukemia by combined all-trans-retinoic acid and idarubicin (AIDA) therapy, Blood, 90, 1014
  7. Marasca, 1999, Missense mutations in the PML/RARα ligand binding domain in ATRA-resistant As2O3 sensitive relapsed acute promyelocytic leukemia, Haematologica, 84, 963
  8. Recchia, 2003, Low dose interleukin-2 and 13-cis-retinoic acid as maintenance therapy in patients with solid tumors responsive to chemotherapy, J. Exp. Clin. Cancer Res, 22, 135
  9. Sun, 1992, treated 32 cases of acute promyelocytic leukemia, Chin. J. Integrat. Chin. West. Med, 12, 170
  10. Thompson, 1997, Retinoic acid-responsive enhancers located 3′ of the hox A and hox B homeobox gene clusters. Functional analysis, J. Biol. Chem, 272, 2167, 10.1074/jbc.272.4.2167 · DOI
  11. Vogel, 1999, Retinoid uptake, metabolism and transport, vol. 139, 31

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Metadata

Authors
di Masi, A., Leboffe, L., De Marinis, E., Pagano, F., Cicconi, L., Rochette-Egly, C., Lo-Coco, F., Ascenzi, P., & Nervi, C.
Affiliations
  • Roma Tre University (IT)
  • Sapienza University of Rome (IT)
  • University of Rome Tor Vergata (IT)
Corresponding author
  • Ascenzi, Paolo
  • Nervi, Clara
ORCID
Venue
Molecular Aspects of Medicine
Publisher
Elsevier BV
Published
2015-02
Volume
41
Pages
1-115
ISSN
0098-2997 (ISSN-L)
DOI
10.1016/j.mam.2014.12.003
OpenAlex
W2064402415
Cited by
403
References
1,341
Citations by year
2026: 20 · 2025: 33 · 2024: 50 · 2023: 32 · 2022: 44 · 2021: 42 · 2020: 41 · 2019: 41 · 2018: 31 · 2017: 24 · 2016: 30 · 2015: 12
FWCI
9.15
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Molecular Aspects of Medicine (publishedVersion)
  • PubMed (publishedVersion)
  • HAL (submittedVersion)
  • Cineca Institutional Research Information System (Tor Vergata University) (submittedVersion)
  • IRIS Research product catalog (Sapienza University of Rome) (submittedVersion)
  • Iris (Roma Tre University) (submittedVersion)
Funders
  • Italian Association for Cancer Research
  • Italian Foundation for Cancer Research (15142)
  • University of Roma “La Sapienza”
  • Fondazione Roma
  • CNRS
  • INSERM
  • Agence Nationale pour la Recherche (ANR-05-BLAN-0390-02, ANR-09-BLAN-0297-01)
  • Foundation pour la Recherche Medicale (DEQ20090515423)
  • Institut National du Cancer (INCa-PLO7-96099, PL09-194)
  • Association pour la Recherche sur le Cancer (3169, SL220110603474)
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 › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
Keywords
retinoic acid receptor, retinoic acid signaling, retinoid X receptor, nuclear receptor superfamily, transcriptional regulation, non-genomic signaling, retinoids, cancer therapy, chemoprevention, leukemia, skin cancer, head and neck cancer, lung cancer, breast cancer, prostate cancer, differentiation therapy, apoptosis
MeSH terms
Retinoic Acid Receptor alpha, Retinoic Acid Receptor gamma, Animals, Antineoplastic Agents, Female, Humans, Male, Neoplasms, Tretinoin, Receptors, Retinoic Acid, Response Elements

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