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Upregulation of annexin A5 affects the biological behaviors of lung squamous carcinoma cells in vitro

查看全文 作  者:Linlin [1]Gong;Haoqi [1]Zhao;Lan [1]Wang;Bing [2]Sun;Lijun [1]Yu;Xiaoyu [1]Qi;Xin [1]Zhou;Liyuan [1]Zhang;Hongwei [3]Guan;Shujuan [1]Shao 高影响力作者 机构地区:[1]Department of Histology and Embryology, Dalian Medical University;[2]Department of Chest Surgery, First Affiliated Hospital of Dalian Medical University;[3]Department of Pathology, First Affiliated Hospital of Dalian Medical University高影响力机构 出  处:《Chinese Science Bulletin》索引2014年第59卷第28期,共11页高影响力期刊 基  金:supported by the National Basic Research Program of China (2012CB967003);National Natural Science Foundation of China (81272225);the Research Fund for the Docoral Program of Higher Education of China (20132106110006);the Science Foundation of Liaoning Province Education Administration (L2013350);Dalian Science Foundation (2011E12SF036). 摘  要:Annexin A5 is a Ca2?-dependent phospholipidbinding protein and protein kinase C inhibitory protein. It has a potential role in cellular signal transduction, inflammation, growth and differentiation. In this study, we evaluated the expression of this protein in lung tumor tissues and subsequently established a NCI-H520 cell line that stably expresses the wild-type ANXA5 gene to determine 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 upregulation of this protein may inhibit the proliferation, migration, and invasion abilities of NCI-H520 cells in vitro. The transfected 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. 关 键 词:膜联蛋白 体外抑制 癌细胞 肺肿瘤 生物学行为 细胞信号转导 PCNA 肿瘤组织
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