Larriba María Jesús, García de Herreros Antonio, Muñoz Alberto
Instituto de Investigaciones Biomédicas "Alberto Sols", Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, IdiPAZ, 28029 Madrid, Spain.
Institut Hospital del Mar d'Investigacions Mèdiques, 08003 Barcelona, Spain; Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra, 08003 Barcelona, Spain.
Stem Cells Int. 2016;2016:6213872. doi: 10.1155/2016/6213872. Epub 2016 Jan 6.
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.
多项研究支持活性维生素D衍生物1α,25 - 二羟基维生素D3（1,25(OH)2D3）与上皮 - 间质转化（EMT）之间的相互调节。因此，1,25(OH)2D3通过诱导多种编码负责上皮表型的细胞黏附及极性蛋白的靶基因，以及抑制关键的EMT诱导因子来抑制EMT。直接和间接调节机制均介导这些效应。相反，某些主要的EMT诱导因子通过抑制编码介导1,25(OH)2D3效应的高亲和力维生素D受体的VDR基因转录，来抑制1,25(OH)2D3的作用。因此，在每种情况下，1,25(OH)2D3信号强度与EMT诱导之间的平衡决定了细胞表型。在此，我们综述了目前对1,25(OH)2D3与EMT相互作用中涉及的基因和机制的理解。
