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

doi:10.1083/jcb.200102028

Published online 16 July 2001. doi:10.1083/jcb.200102028

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© The Rockefeller University Press, 0021-9525/2001/7/369 $5.00
The Journal of Cell Biology, Volume 154, Number 2, July 23, 2001 369-388

Article

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

Héctor G. Pálmer¹, José Manuel González-Sancho¹, Jesús Espada¹, María T. Berciano², Isabel Puig³, Josep Baulida³, Miguel Quintanilla¹, Amparo Cano¹, Antonio García de Herreros³, Miguel Lafarga² and Alberto Muñoz¹

¹ Instituto de Investigaciones Biomédicas "Alberto Sols, " Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid, E-28029 Madrid, Spain
² Departamento de Anatomía y Biología Celular, Universidad de Cantabria, E-39011 Santander, Spain
³ Unitat de Biologia Celular i Molecular, Institut Municipal Investigació Mèdica, Universitat Pompeu Fabra, E-08003 Barcelona, Spain

Address correspondence to Alberto Muñoz, Instituto de Investigaciones Biomédicas "Alberto Sols," Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid, Arturo Duperier 4, E-28029 Madrid, Spain. Tel.: 34-91-5854640. Fax: 34-91-5854587. E-mail: amunoz{at}iib.uam.es

The ß-catenin signaling pathway is deregulated innearly all colon cancers. Nonhypercalcemic vitamin D3 (1 ${alpha}$ ,25-dehydroxyvitaminD₃) analogues are candidate drugs to treat this neoplasia. Weshow that these compounds promote the differentiation of humancolon carcinoma SW480 cells expressing vitamin D receptors (VDRs)(SW480-ADH) but not that of a malignant subline (SW480-R) ormetastasic derivative (SW620) cells lacking VDR. 1 ${alpha}$ ,25(OH)₂D₃induced the expression of E-cadherin and other adhesion proteins(occludin, Zonula occludens [ZO]-1, ZO-2, vinculin) and promotedthe translocation of ß-catenin, plakoglobin, and ZO-1from the nucleus to the plasma membrane. Ligand-activated VDRcompeted with T cell transcription factor (TCF)-4 for ß-cateninbinding. Accordingly, 1 ${alpha}$ ,25(OH)₂D₃ repressed ß-catenin–TCF-4transcriptional activity. Moreover, VDR activity was enhancedby ectopic ß-catenin and reduced by TCF-4. Also, 1 ${alpha}$ ,25(OH)₂D₃inhibited expression of ß-catenin–TCF-4-responsivegenes, c-myc, peroxisome proliferator-activated receptor ${delta}$ , Tcf-1,and CD44, whereas it induced expression of ZO-1. Our resultsshow that 1 ${alpha}$ ,25(OH)₂D₃ induces E-cadherin and modulates ß-catenin–TCF-4target genes in a manner opposite to that of ß-catenin,promoting the differentiation of colon carcinoma cells.

Key Words: vitamin D; vitamin D receptor; ß-catenin; E-cadherin; colon cancer

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