| dc.creator |
Pálmer, Héctor G. |
|
| dc.creator |
González-Sancho, José Manuel |
|
| dc.creator |
Espada, Jesús |
|
| dc.creator |
Berciano, María T. |
|
| dc.creator |
Quintanilla, Miguel |
|
| dc.creator |
Cano, Amparo |
|
| dc.creator |
Lafarga, Miguel |
|
| dc.creator |
Muñoz Terol, Alberto |
|
| dc.date |
2008-06-26T09:34:13Z |
|
| dc.date |
2008-06-26T09:34:13Z |
|
| dc.date |
2001-07-23 |
|
| dc.date.accessioned |
2017-01-31T01:55:12Z |
|
| dc.date.available |
2017-01-31T01:55:12Z |
|
| dc.identifier |
Journal of Cell Biology 154(2): 369–388 (2001) |
|
| dc.identifier |
0021-9525 |
|
| dc.identifier |
http://hdl.handle.net/10261/5361 |
|
| dc.identifier |
10.1083/jcb.200102028 |
|
| dc.identifier.uri |
http://dspace.mediu.edu.my:8181/xmlui/handle/10261/5361 |
|
| dc.description |
et al. |
|
| dc.description |
The 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. |
|
| dc.description |
H.G. Pálmer and J.M. González-Sancho were recipients of fellowships from the Comunidad Autónoma de Madrid. This work was supported by a grant from the Plan Nacional de Investigación y Desarrollo (SAF98-0060), Ministerio de Ciencia y Tecnología of Spain. |
|
| dc.description |
Peer reviewed |
|
| dc.format |
1043527 bytes |
|
| dc.format |
application/pdf |
|
| dc.language |
eng |
|
| dc.publisher |
Rockefeller University Press |
|
| dc.relation |
http://dx.doi.org/10.1083/jcb.200102028 |
|
| dc.rights |
openAccess |
|
| dc.subject |
Vitamin D |
|
| dc.subject |
Vitamin D receptor |
|
| dc.subject |
β-catenin |
|
| dc.subject |
E-cadherin |
|
| dc.subject |
Colon cancer |
|
| dc.title |
Vitamin D3 promotes the differentiation of colon carcinoma cells by the induction of E-cadherin and the inhibition of β-catenin signaling |
|
| dc.type |
Artículo |
|