Abstract
Aurora kinases play key roles in the transition of G2/M phase by regulating functions of centrosomes and microtubules. Overexpression of Aurora-A, a new oncogene, can induce centrosome amplification, aneuploidy and tumor formation. Aurora kinases are closely associated with breast cancer. In this article, we reviewed the mechanisms of Aurora kinases inducing tumorigenesis of breast cancer via interacting with p53 gene, BRCA1 gene, PTEN/PI3K/AKT pathway, gene polymorphism, estrogen, and so on, analyzed the expression of Aurora kinases in breast cancer and its relationship with prognosis.
MeSH terms
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Animals
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Aurora Kinases
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Breast Neoplasms / etiology
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Breast Neoplasms / genetics
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Breast Neoplasms / metabolism*
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Carcinoma in Situ / etiology
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Carcinoma in Situ / genetics
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Carcinoma in Situ / metabolism
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Carcinoma, Ductal, Breast / etiology
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Carcinoma, Ductal, Breast / genetics
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Carcinoma, Ductal, Breast / metabolism*
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Cell Transformation, Neoplastic
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Estrogens / metabolism
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Female
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Humans
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PTEN Phosphohydrolase / metabolism
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Phosphatidylinositol 3-Kinases / metabolism
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Polymorphism, Genetic
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Prognosis
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Protein Serine-Threonine Kinases / genetics
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Protein Serine-Threonine Kinases / metabolism*
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Protein Serine-Threonine Kinases / physiology
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Proto-Oncogene Proteins c-akt / metabolism
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Signal Transduction
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Tumor Suppressor Protein p53 / metabolism
Substances
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Estrogens
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Tumor Suppressor Protein p53
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Aurora Kinases
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Protein Serine-Threonine Kinases
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Proto-Oncogene Proteins c-akt
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PTEN Phosphohydrolase
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PTEN protein, human