Vitamin D and the Epithelial to Mesenchymal Transition

Several studies support reciprocal regulation between the active vitamin D derivative 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3) and the epithelial to mesenchymal transition (EMT). Thus, 1,25(OH)2D3 inhibits EMT via the induction of a variety of target genes that encode cell adhesion and polarity prote...

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Main Authors: María Jesús Larriba, Antonio García de Herreros, Alberto Muñoz
Format: Article
Language:English
Published: Hindawi Limited 2016-01-01
Series:Stem Cells International
Online Access:http://dx.doi.org/10.1155/2016/6213872
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spelling doaj-7b8c899cd6214e7fadf8940c56fdd4af2020-11-24T23:59:33ZengHindawi LimitedStem Cells International1687-966X1687-96782016-01-01201610.1155/2016/62138726213872Vitamin D and the Epithelial to Mesenchymal TransitionMaría Jesús Larriba0Antonio García de Herreros1Alberto Muñoz2Instituto de Investigaciones Biomédicas “Alberto Sols”, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, IdiPAZ, 28029 Madrid, SpainInstitut Hospital del Mar d’Investigacions Mèdiques, 08003 Barcelona, SpainInstituto de Investigaciones Biomédicas “Alberto Sols”, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, IdiPAZ, 28029 Madrid, SpainSeveral studies support reciprocal regulation between the active vitamin D derivative 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3) and the epithelial to mesenchymal transition (EMT). Thus, 1,25(OH)2D3 inhibits EMT via the induction of a variety of target genes that encode cell adhesion and polarity proteins responsible for the epithelial phenotype and through the repression of key EMT inducers. Both direct and indirect regulatory mechanisms mediate these effects. Conversely, certain master EMT inducers inhibit 1,25(OH)2D3 action by repressing the transcription of VDR gene encoding the high affinity vitamin D receptor that mediates 1,25(OH)2D3 effects. Consequently, the balance between the strength of 1,25(OH)2D3 signaling and the induction of EMT defines the cellular phenotype in each context. Here we review the current understanding of the genes and mechanisms involved in the interplay between 1,25(OH)2D3 and EMT.http://dx.doi.org/10.1155/2016/6213872
collection DOAJ
language English
format Article
sources DOAJ
author María Jesús Larriba
Antonio García de Herreros
Alberto Muñoz
spellingShingle María Jesús Larriba
Antonio García de Herreros
Alberto Muñoz
Vitamin D and the Epithelial to Mesenchymal Transition
Stem Cells International
author_facet María Jesús Larriba
Antonio García de Herreros
Alberto Muñoz
author_sort María Jesús Larriba
title Vitamin D and the Epithelial to Mesenchymal Transition
title_short Vitamin D and the Epithelial to Mesenchymal Transition
title_full Vitamin D and the Epithelial to Mesenchymal Transition
title_fullStr Vitamin D and the Epithelial to Mesenchymal Transition
title_full_unstemmed Vitamin D and the Epithelial to Mesenchymal Transition
title_sort vitamin d and the epithelial to mesenchymal transition
publisher Hindawi Limited
series Stem Cells International
issn 1687-966X
1687-9678
publishDate 2016-01-01
description Several studies support reciprocal regulation between the active vitamin D derivative 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3) and the epithelial to mesenchymal transition (EMT). Thus, 1,25(OH)2D3 inhibits EMT via the induction of a variety of target genes that encode cell adhesion and polarity proteins responsible for the epithelial phenotype and through the repression of key EMT inducers. Both direct and indirect regulatory mechanisms mediate these effects. Conversely, certain master EMT inducers inhibit 1,25(OH)2D3 action by repressing the transcription of VDR gene encoding the high affinity vitamin D receptor that mediates 1,25(OH)2D3 effects. Consequently, the balance between the strength of 1,25(OH)2D3 signaling and the induction of EMT defines the cellular phenotype in each context. Here we review the current understanding of the genes and mechanisms involved in the interplay between 1,25(OH)2D3 and EMT.
url http://dx.doi.org/10.1155/2016/6213872
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