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首页> 外文期刊>Genes to cells : >Over-expression of Aurora-A targets cytoplasmic polyadenylation element binding protein and promotes mRNA polyadenylation of Cdk1 and cyclin B1.
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Over-expression of Aurora-A targets cytoplasmic polyadenylation element binding protein and promotes mRNA polyadenylation of Cdk1 and cyclin B1.

机译：Aurora-A的过表达靶向细胞质聚腺苷酸化元素结合蛋白，并促进Cdk1和细胞周期蛋白B1的mRNA聚腺苷酸化。

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摘要

Aurora-A is a centrosomal serine-threonine kinase that regulates mitosis. Over-expression of Aurora-A has been found in a wide range of tumors and has been implicated in oncogenic transformation. However, how Aurora-A over-expression contributes to promotion of carcinogenesis remains elusive. Immunohistochemical analysis of breast tumors revealed that over-expressed Aurora-A is not restricted to the centrosomes but is also found in the cytoplasm. This over-expressed Aurora-A appeared to be phosphorylated on Thr288, which is known to be required for its enzymatic activation. In analogy to Aurora-A's role in oocyte maturation and the early embryonic cell cycle, here we investigated whether ectopically over-expressed Aurora-A can similarly stimulate polyadenylation of mRNA in human somatic cultured cells by interacting with a human ortholog of cytoplasmic polyadenylation element binding protein, h-CPEB. In vitro experiments revealed that Aurora-A binds directly to, and phosphorylates, h-CPEB. We found that polyadenylation of mRNA tails of cyclin B1 and Cdk1 was synergistically stimulated when Aurora-A and h-CPEB were over-expressed, and they were further promoted in the presence of an Aurora-A activator Ajuba. Our results suggest a function of ectopically over-expressed Aurora-A that might be relevant for carcinogenesis.
机译：Aurora-A是一种调节有丝分裂的中心体丝氨酸-苏氨酸激酶。在多种肿瘤中都发现了Aurora-A的过度表达，并与致癌转化有关。然而，极光-A过度表达如何促进癌变仍不清楚。乳腺肿瘤的免疫组织化学分析显示，过度表达的Aurora-A不仅限于中心体，而且还存在于细胞质中。这种过度表达的Aurora-A似乎在Thr288上被磷酸化，这被认为是其酶促活化所必需的。类似于Aurora-A在卵母细胞成熟和早期胚胎细胞周期中的作用，在这里我们研究了异位过量表达的Aurora-A是否可以通过与人类胞质多腺苷酸化因子结合的直系同源物相互作用来刺激人类体细胞培养细胞中mRNA的多腺苷酸化。蛋白，h-CPEB。体外实验表明，Aurora-A直接与h-CPEB结合并使其磷酸化。我们发现当Aurora-A和h-CPEB过度表达时，细胞周期蛋白B1和Cdk1的mRNA尾巴的多腺苷酸被协同刺激，在存在Aurora-A激活剂Ajuba的情况下，它们进一步被促进。我们的结果表明异位过表达的Aurora-A的功能可能与致癌作用有关。

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