Abstract
Aurora family of protein kinases have emerged as crucial factors of, not only mitosis and cytokinesis, but also human carcinogenesis. Among these family members is Aurora-A that is frequently overexpressed in varieties of human cancer. Both in vitro and in vivo studies demonstrated that Aurora-A induces tumorigenesis through genome instability. These studies have further shown that cell signaling cross-talk between Aurora-A and other cellular proteins are essential for fully-transformed phenotypes. This review summarizes recent progress of Aurora-A-associated carcinogenesis.
Keywords:
Aurora-A; Cell Cycle; Checkpoint; Genome Instability; Phosphorylation; Plk1; mTOR.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Aurora Kinases
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BRCA1 Protein / metabolism
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Cell Cycle Proteins / metabolism
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Cell Transformation, Neoplastic*
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Humans
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Intracellular Signaling Peptides and Proteins / metabolism
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Neoplasms / enzymology*
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Neoplasms / genetics
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Neoplasms / metabolism
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Polo-Like Kinase 1
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Protein Serine-Threonine Kinases / metabolism*
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Proto-Oncogene Proteins / metabolism
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Signal Transduction
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TOR Serine-Threonine Kinases
Substances
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BRCA1 Protein
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Cell Cycle Proteins
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Intracellular Signaling Peptides and Proteins
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Proto-Oncogene Proteins
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MTOR protein, human
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Aurora Kinases
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Protein Serine-Threonine Kinases
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TOR Serine-Threonine Kinases