Abstract
We determined the molecular mechanism of inhibitory effect of human mesenchymal stem cells (hMSCs) on the growth of human MCF-7 breast cancer cells. Our finding showed that beta-catenin was down-regulated in MCF-7 cells by conditioned media from Z3 hMSCs, and the expression level of dickkopf-1 (Dkk-1) was higher in Z3 cells than that in MCF-7 cells. Neutralization of Dkk-1 and small interference RNA targeting Dkk-1 mRNA in Z3 cells attenuated the inhibitory effect of Z3 cells on MCF-7 cells. Overexpression of Dkk-1 in Z3 cells enhanced the inhibition. Therefore, Dkk-1 secreted by Z3 cells involves the inhibition via the Wnt pathway.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Breast Neoplasms / pathology
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Breast Neoplasms / prevention & control*
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Cell Proliferation
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Cells, Cultured
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Culture Media, Conditioned
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Humans
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Intercellular Signaling Peptides and Proteins / analysis
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Intercellular Signaling Peptides and Proteins / genetics
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Intercellular Signaling Peptides and Proteins / physiology*
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Mesenchymal Stem Cells / physiology*
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Mice
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Mice, SCID
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Signal Transduction / physiology*
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Wnt Proteins / antagonists & inhibitors
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Wnt Proteins / physiology*
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beta Catenin / physiology
Substances
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Culture Media, Conditioned
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DKK1 protein, human
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Intercellular Signaling Peptides and Proteins
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Wnt Proteins
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beta Catenin