中文摘要：

Annexin A5 是 Ca < 啜 class= “ a-plus-plus ” >2+-dependent phospholipid 有约束力的蛋白质和蛋白质 kinase C 禁止的蛋白质。它在细胞的信号 transduction，发炎，生长和区别有一个潜在的角色。在这研究，我们在肺肿瘤纸巾计算了这蛋白质的表达式并且随后建立了稳定地表示野类型的 ANXA5 基因在 vitro 在房间形态学，增长和转移潜力上决定 annexin A5 upregulation 的效果的一根 NCI-H520 房间线。NCI-H520 房间上的 annexin A5 的效果被水晶测试紫染色， CCK-8 试金，擦伤创伤试金，和 Transwell 试金。Akt， PCNA， vimentin，和 E-cadherin 的表情被西方的污点试金检验。在这研究，我们证明 annexin A5 与正常纸巾相比在肿瘤纸巾在底层被表示。另外，这蛋白质的 upregulation 可以在 vitro 禁止 NCI-H520 房间的增长，迁居，和侵略能力。transfected 房间在 G 被逮捕 < 潜水艇 class= “ a-plus-plus ” > 房间周期的 1 个 /S 阶段，和 Akt， PCNA 和 Vimentin 的表示层次是 downregulated，当 E-cadherin 是 upregulated 时。

英文摘要：

Annexin A5 is a Ca2＋-dependent phospholipid- binding protein and protein kinase C inhibitory protein. It has a potential role in cellular signal transduction, inflam- mation, growth and differentiation. In this study, we evaluated the expression of this protein in lung tumor tis- sues and subsequently established a NCI-H520 cell line that stably expresses the wild-type ANXA5 gene to deter- mine the effects of annexin A5 upregulation on the cell morphology, proliferation and metastasis potential in vitro. The effects of annexin A5 on NCI-H520 cells were tested by crystal violet staining, CCK-8 assay, scratch wound assay, and Transwell assay. The expressions of Akt, PCNA, vimentin, and E-cadherin were examined by Western blot assay. In this study, we demonstrated that annexin A5 is expressed at lower levels in tumor tissues compared with normal tissues. Additionally, the upregu- lation of this protein may inhibit the proliferation, migra- tion, and invasion abilities of NCI-H520 cells in vitro. Thetransfected cells were arrested in the G1/S phase of the cell cycle, and the expression levels of Akt, PCNA and Vimentin were downregulated, while E-cadherin was upregulated.