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RhoA-ROCK and p38MAPK-MSK1 mediate vitamin D effects on gene expression, phenotype, and Wnt pathway in colon cancer cells

AuthorsOrdóñez-Morán, Paloma ; Larriba, María Jesús ; Pálmer, Héctor G.; Valero, Ruth A. ; Barbáchano, Antonio ; Duñach, Mireia; Villalobos, Carlos ; Berciano, María T.; Lafarga, Miguel; Muñoz Terol, Alberto
Signaling pathways
25-dihydroxyvitamin d-3
Issue Date17-Nov-2008
PublisherRockefeller University Press
CitationJournal of Cell Biology 183(4): 697-719 (2008)
AbstractThe active vitamin D metabolite 1,25-dihydroxy-vitamin D-3 (1,25(OH)(2)D-3) inhibits proliferation and promotes differentiation of colon cancer cells through the activation of vitamin D receptor (VDR), a transcription factor of the nuclear receptor superfamily. Additionally, 1,25(OH)(2)D-3 has several nongenomic effects of uncertain relevance. We show that 1,25(OH)(2)D-3 induces a transcription-independent Ca2+ influx and activation of RhoA-Rho-associated coiled kinase (ROCK). This requires VDR and is followed by activation of the p38 mitogen-activated protein kinase (p38MAPK) and mitogen- and stress-activated kinase 1 (MSK1). As shown by the use of chemical inhibitors, dominant-negative mutants and small interfering RNA, RhoA-ROCK, and p38MAPK-MSK1 activation is necessary for the induction of CDH1/E-cadherin, CYP24, and other genes and of an adhesive phenotype by 1,25(OH)(2)D-3. RhoA-ROCK and MSK1 are also required for the inhibition of Wnt-beta-catenin pathway and cell proliferation. Thus, the action of 1,25( OH) 2 D 3 on colon carcinoma cells depends on the dual action of VDR as a transcription factor and a nongenomic activator of RhoA-ROCK and p38MAPK-MSK1
Publisher version (URL)http://dx.doi.org/10.1083/jcb.200803020
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