Abstract
The microRNA miR-9 is induced by Myc in breast cancer cells where it targets the major epithelial adherens junction protein, E-cadherin. This primes the cancer cells for epithelial-mesenchymal transition (EMT) and also stimulates angiogenesis in tumours.
MeSH terms
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Animals
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Antigens, CD
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Breast Neoplasms / metabolism
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Breast Neoplasms / pathology
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Cadherins / genetics
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Cadherins / metabolism
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Cell Proliferation
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Cell Transdifferentiation / genetics
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Down-Regulation / genetics
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Female
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Gene Expression Regulation, Neoplastic / physiology*
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Humans
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Mice
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MicroRNAs / antagonists & inhibitors
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MicroRNAs / physiology*
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Models, Biological
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N-Myc Proto-Oncogene Protein
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Neoplasm Invasiveness / genetics
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Neoplasm Invasiveness / pathology
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Neoplasm Metastasis / genetics*
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Neoplasm Metastasis / pathology
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Neoplasms / metabolism
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Neoplasms / pathology
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Neovascularization, Pathologic / metabolism
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Neovascularization, Pathologic / pathology
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Neuroblastoma / metabolism
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Nuclear Proteins / genetics
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Nuclear Proteins / metabolism
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Oncogene Proteins / genetics
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Oncogene Proteins / metabolism
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Proto-Oncogene Proteins c-myc / genetics
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Proto-Oncogene Proteins c-myc / metabolism*
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Signal Transduction / physiology
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Transplantation, Heterologous / pathology
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Vascular Endothelial Growth Factor A / blood
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Vascular Endothelial Growth Factor A / genetics
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Vimentin / metabolism
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beta Catenin / genetics
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beta Catenin / metabolism
Substances
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Antigens, CD
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CDH1 protein, human
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CTNNB1 protein, human
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Cadherins
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MIRN92 microRNA, human
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MYCN protein, human
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MicroRNAs
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N-Myc Proto-Oncogene Protein
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Nuclear Proteins
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Oncogene Proteins
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Proto-Oncogene Proteins c-myc
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VEGFA protein, human
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Vascular Endothelial Growth Factor A
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Vimentin
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beta Catenin