中文摘要：

食道的有鳞的房间癌(ESCC ) 是最普通的恶意之一。识别预言肿瘤前进和治疗学的分子的目标的新 markersfor 是必要的。它被报导了 Aurora-Aand 矩阵 metalloproteinases 的那 overexpressions (MMP-2 ) 2 可以支持肿瘤的恶意的发展。然而，关系 betweenAurora -- 在肿瘤病人的 A 和 MMP-2 表示没被调查。另外， Aurora-Aregulates MMP-2 表示不充分仍然是的内在的机制阐明了。在这研究，我们表明了那曙光 A， MMP-2 与配对的正常邻近的纸巾相比是 overexpressedin ESCC 纸巾(P ?

英文摘要：

Esophageal squamous cell carcinoma （ESCC） is one of the most common malignancies. It is necessary to identify new markers for predicting tumor progression and therapeutic molecular targets. It has been reported that overexpressions of Aurora-A and matrix metalloproteinases 2 （MMP-2） may promote the malignant development of tumor. However, the relationship between Aurora-A and MMP-2 expression in tumor patients has not been investigated. In addition, the underlying mechanisms that Aurora-A regulates MMP-2 expression are still not fully elucidated. In this study, we demonstrated that Aurora-A and MMP-2 were overexpressed in ESCC tissues compared with paired normal adjacent tissues （P 〈 0.0001）. Overexpression of Aurora-A was associated with the lymph node metastasis of ESCC （P = 0.01）. Significantly, Aurora-A protein expression was positively correlated with MMP-2 protein expression in ESCC tissues （r = 0.66, P 〈 0.0001） as well as in ESCC cell lines. The level of Aurora-A expression was also positively correlated with the invasion capability of ESCC cells. Furthermore, Aurora-A overexpression significantly increased ESCC cell invasion by the upregulation of MMP-2 expression. In addition, Aurora-A overexpression promoted nuclear factor-kappaB （NF-κB） activation, and Aurora-Amediated MMP-2 upregulation was abrogated by NF-κB inhibitor. Further analysis showed that activation of NF-κB was severely attenuated by AKT inhibitor in cells overexpressing Aurora-A. Taken together, these data indicate that Aurora-A overexpression upregulates MMP-2 expression through activating AKT/NF-κB signaling pathway in ESCC cells. These findings reveal that Aurora-A may be used as an important indicator for the judgment of malignant behavior of ESCC, and may be an attractive target for cancer therapy.