Journal
CANCERS
Volume 12, Issue 9, Pages -Publisher
MDPI
DOI: 10.3390/cancers12092413
Keywords
vitamin D; cell differentiation; stemness; cancer; carcinoma cells; cancer-associated fibroblasts; cancer stem cells; organoids; epithelial-mesenchymal transition; Wnt/beta-catenin
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Funding
- Agencia Estatal de Investigacion [PID2019-104867RB-I00/AEI/10.13039/501100011033]
- Agencia Estatal de Investigacion-Fondo Europeo de Desarrollo Regional (MINECO/AEI/FEDER, EU) [SAF2016-76377-R]
- Instituto de Salud Carlos III-Fondo Europeo de Desarrollo Regional (CIBERONC) [CB16/12/00273]
- Ministerio de Economia y Competitividad [SAF2017-90604-REDT/NuRCaMeIn]
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Vitamin D(3)is the precursor of 1 alpha,25-dihydroxyvitamin D-3(1,25(OH)(2)D-3), a pleiotropic hormone that is a major regulator of the human genome. 1,25(OH)(2)D(3)modulates the phenotype and physiology of many cell types by controlling the expression of hundreds of genes in a tissue- and cell-specific fashion. Vitamin D deficiency is common among cancer patients and numerous studies have reported that 1,25(OH)(2)D(3)promotes the differentiation of a wide panel of cultured carcinoma cells, frequently associated with a reduction in cell proliferation and survival. A major mechanism of this action is inhibition of the epithelial-mesenchymal transition, which in turn is largely based on antagonism of the Wnt/beta-catenin, TGF-beta and EGF signaling pathways. In addition, 1,25(OH)(2)D(3)controls the gene expression profile and phenotype of cancer-associated fibroblasts (CAFs), which are important players in the tumorigenic process. Moreover, recent data suggest a regulatory role of 1,25(OH)(2)D(3)in the biology of normal and cancer stem cells (CSCs). Here, we revise the current knowledge of the molecular and genetic basis of the regulation by 1,25(OH)(2)D(3)of the differentiation and stemness of human carcinoma cells, CAFs and CSCs. These effects support a homeostatic non-cytotoxic anticancer action of 1,25(OH)(2)D(3)based on reprogramming of the phenotype of several cell types.
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