From molecular basis to clinical insights: a challenging future for the vitamin D endocrine system in colorectal cancer
Entity
UAM. Departamento de BioquímicaPublisher
WileyDate
2023-09-12Citation
10.1111/febs.16955
The FEBS Journal (2023): 1-34
ISSN
1742-464X (print); 1742-4658 (online)DOI
10.1111/febs.16955Funded by
The work in the authors laboratory is funded by the Agencia Estatal de Investigacion (PID2019-104867RB-I00 and PID2022-136729OB-I00; MCIN/AEI/ 10.13039/501100011033), the Instituto de Salud Carlos III – Fondo Europeo de Desarrollo Regional (CIBERONC/CB16/12/00273 and ICI20/00057), and the Comunidad de Madrid (S2022/BMD-7212). AF-B, MJL, AB, and JMG-S belong to the Spanish National Research Council (CSIC)’s Cancer HubProject
Gobierno de España. PID2019-104867RB-100; Gobierno de España. PID2022-136729OB-I00Editor's Version
https://doi.org/10.1111/febs.16955Subjects
Colorectal cancer; Epidemiology; Mechanisms of action; Randomized controlled trials; Vitamin D; MedicinaRights
© 2023 The AuthorsAbstract
Colorectal cancer (CRC) is one of the most life-threatening neoplasias in
terms of incidence and mortality worldwide. Vitamin D deficiency has been
associated with an increased risk of CRC. 1a,25-Dihydroxyvitamin D3
[1,25(OH)2D3], the most active vitamin D metabolite, is a pleiotropic hormone that, through its binding to a transcription factor of the nuclear
receptor superfamily, is a major regulator of the human genome. 1,25
(OH)2D3 acts on colon carcinoma and stromal cells and displays tumor
protective actions. Here, we review the variety of molecular mechanisms
underlying the effects of 1,25(OH)2D3 in CRC, which affect multiple processes that are dysregulated during tumor initiation and progression. Additionally, we discuss the epidemiological data that associate vitamin D
deficiency and CRC, and the most relevant randomized controlled trials of
vitamin D3 supplementation conducted in both healthy individuals and
CRC patients
Files in this item
Google Scholar:Pereira, Fábio
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Fernández Barral, Asunción
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Larriba, María Jesús
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Barbáchano, Antonio
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González Sancho, José Manuel
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