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MicroRNA-22 is induced by vitamin D and contributes to its antiproliferative, antimigratory and gene regulatory effects in colon cancer cells

AuthorsÁlvarez-Díaz, S.; Valle, Noelia ; Ferrer-Mayorga, Gemma ; Lombardía, Luis; Herrera, Mercedes; Domínguez, Orlando; Segura, Miguel F.; Bonilla, Félix; Hernando, Eva; Muñoz Terol, Alberto
Issue Date10-Feb-2012
PublisherOxford University Press
CitationHuman Molecular Genetics 21(10): 2157-2165 (2012)
AbstractVitamin D deficiency is associated with the high risk of colon cancer and a variety of other diseases. The active vitamin D metabolite 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3) regulates gene transcription via its nuclear receptor (VDR), and posttranscriptional regulatory mechanisms of gene expression have also been proposed. We have identified microRNA-22 (miR-22) and several other miRNA species as 1,25(OH)2D3 targets in human colon cancer cells. Remarkably, miR-22 is induced by 1,25(OH)2D3 in a time-, dose- and VDR-dependent manner. In SW480-ADH and HCT116 cells, miR-22 loss-of-function by transfection of a miR-22 inhibitor suppresses the antiproliferative effect of 1,25(OH)2D3. Additionally, miR-22 inhibition increases cell migration per se and decreases the antimigratory effect of 1,25(OH)2D3 in both cell types. In silico analysis shows a significant overlap between genes suppressed by 1,25(OH)2D3 and miR-22 putative target genes. Consistently, miR-22 inhibition abrogates the 1,25(OH)2D3-mediated suppression of NELL2, OGN, HNRPH1, RERE and NFAT5 genes. In 39 out of 50 (78%) human colon cancer patients, miR-22 expression was found lower in the tumour than in the matched normal tissue and correlated directly with that of VDR. Our results indicate that miR-22 is induced by 1,25(OH)2D3 in human colon cancer cells and it may contribute to its antitumour action against this neoplasia.
DescriptionThis is a pre-copy-editing, author-produced PDF of an article accepted for publication in Human Molecular Genetics following peer review.
Publisher version (URL)http://dx.doi.org/10.1093/hmg/dds031
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