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Vitamin D3 promotes the differentiation of colon carcinoma cells by the induction of E-cadherin and the inhibition of β-catenin signaling

AutorPálmer, Héctor G.; González-Sancho, José Manuel ; Espada, Jesús ; Berciano, María T.; Quintanilla, Miguel ; Cano, Amparo ; Lafarga, Miguel; Muñoz Terol, Alberto
Palabras claveVitamin D
Vitamin D receptor
β-catenin
E-cadherin
Colon cancer
Fecha de publicación23-jul-2001
EditorRockefeller University Press
CitaciónJournal of Cell Biology 154(2): 369–388 (2001)
ResumenThe β-catenin signaling pathway is deregulated in nearly all colon cancers. Nonhypercalcemic vitamin D3 (1α,25-dehydroxyvitamin D3) analogues are candidate drugs to treat this neoplasia. We show that these compounds promote the differentiation of human colon carcinoma SW480 cells expressing vitamin D receptors (VDRs) (SW480-ADH) but not that of a malignant subline (SW480-R) or metastasic derivative (SW620) cells lacking VDR. 1α,25(OH)2D3 induced the expression of E-cadherin and other adhesion proteins (occludin, Zonula occludens [ZO]-1, ZO-2, vinculin) and promoted the translocation of β-catenin, plakoglobin, and ZO-1 from the nucleus to the plasma membrane. Ligand-activated VDR competed with T cell transcription factor (TCF)-4 for β-catenin binding. Accordingly, 1α,25(OH)2D3 repressed β-catenin–TCF-4 transcriptional activity. Moreover, VDR activity was enhanced by ectopic β-catenin and reduced by TCF-4. Also, 1α,25(OH)2D3 inhibited expression of β-catenin–TCF-4-responsive genes, c-myc, peroxisome proliferator-activated receptor δ, Tcf-1, and CD44, whereas it induced expression of ZO-1. Our results show that 1α,25(OH)2D3 induces E-cadherin and modulates β-catenin–TCF-4 target genes in a manner opposite to that of β-catenin, promoting the differentiation of colon carcinoma cells.
Descripciónet al.
Versión del editorhttp://dx.doi.org/10.1083/jcb.200102028
URIhttp://hdl.handle.net/10261/5361
DOI10.1083/jcb.200102028
ISSN0021-9525
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