Abstract
Here in, we investigated the mechanism underlying overexpression of miR-135b in the human head and neck squamous cell carcinoma (HNSCC) cell lines and in the HNSCC mouse model. Exogenous expression of miR-135b in these cell lines increased cell proliferation, migration, and colony formation. Gene silencing analysis revealed that miR-135b affects a regulator that inhibits hypoxia-inducible factor (HIF). Increased miR-135b expression was positively correlated with HIF-1α expression and microvessel density in the HNSCC model. Thus, our data demonstrate that miR-135b acts as a tumor promoter by promoting cancer cell proliferation, colony formation, survival, and angiogenesis through activation of HIF-1α in HNSCC.
Published by Elsevier Ireland Ltd.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Blotting, Western
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Carcinoma, Squamous Cell / genetics
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Carcinoma, Squamous Cell / metabolism*
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Carcinoma, Squamous Cell / pathology
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Cell Proliferation
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Cells, Cultured
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Disease Models, Animal
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Gene Deletion
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Head and Neck Neoplasms / genetics
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Head and Neck Neoplasms / metabolism*
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Head and Neck Neoplasms / pathology
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Humans
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Hypoxia-Inducible Factor 1 / metabolism*
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Mice
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Mice, Knockout
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MicroRNAs / physiology*
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PTEN Phosphohydrolase / genetics
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Protein Serine-Threonine Kinases / genetics
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Real-Time Polymerase Chain Reaction
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Receptor, Transforming Growth Factor-beta Type I
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Receptors, Transforming Growth Factor beta / genetics
Substances
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Hypoxia-Inducible Factor 1
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MicroRNAs
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Mirn135 microRNA, mouse
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Receptors, Transforming Growth Factor beta
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Protein Serine-Threonine Kinases
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Receptor, Transforming Growth Factor-beta Type I
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PTEN Phosphohydrolase
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Pten protein, mouse