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| DC Field | Value | Language |
|---|---|---|
| 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 | - |
| Appears in Collections: | Digital Csic | |
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