作者: Adrianne E. Hontz , Sara A. Li , Jeffrey L. Salisbury , Wilma L. Lingle , Jonathan J. Li
DOI: 10.1007/978-0-387-69080-3_39
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摘要: Sustained over-expression of Aurora A (AurA), centrosome amplification, chromosomal instability, and aneuploidy are salient features that occur in high frequency human breast premalignant stages primary ductal cancer (BC), as well 17β-estradiol (E2)-induced oncogenesis animal models. We have reported AurA/B protein expression increases 8.7-and 4.6-fold, respectively, E2-induced male Syrian hamster uterine stem cell-like tumors the kidney (EUTK) when compared with cholesterol-treated control kidneys. Upon a 10-day E2-withdrawal or coadministration tamoxifen citrate, 78–79% 81–64% reduction expression, were observed from animals continuously exposed to E2. These data indicate is regulated by estrogens via estrogen receptor a. To determine whether this Aur kinases may contribute alterations during their phosphorylation specific substrates, we analyzed histone H3 targeting for Xklp2 (TPX2). Histone TPX2 significantly over-expressed 3.7- 1.6-fold, samples. Immunohistochemistry revealed was essentially confined tumor foci cells. Collectively, these under deregulation kinase substrates implicated eliciting oncogenesis.