Cyclin-dependent kinase 2-associated protein 1（CDK2AP1）, a cell growth inhibitory factor, is abnormally expressed in cancer cells, and might be implicated in the development of lung cancer. However, no studies on th...Cyclin-dependent kinase 2-associated protein 1（CDK2AP1）, a cell growth inhibitory factor, is abnormally expressed in cancer cells, and might be implicated in the development of lung cancer. However, no studies on the function of CDK2AP1 in human lung cancer have been yet reported. In this study, overexpressing lentiviral vectors containing full-length CDK2AP1 cDNA and CDK2AP1 shRNA（short hairpin RNA） were constructed. Our results show that infecting A549 cells with lentivirus containing CDK2AP1 shRNA or full-length CDK2AP1 cDNA results in significantly down- or up-regulated the expression of CDK2AP1, respectively, thereby providing reliable tools for studying the function of CDK2AP1 in pulmonary carcinogenesis. Our data of MTT assay and flowcytometric analysis demonstrate that CDK2AP1 plays an important role in the proliferation/growth and cell cycling of A549 cells in vitro, and further investigation into its underlying mechanism of pulmonary carcinogenesis is needed.展开更多
基金Supported by the Grants from the Project of Scientific Innovation and Creative for Jilin Provincial Oversea Scholars(No.2010273)Jilin Provincial Science and Technology Services(Nos.20050408, 20070720, 200805120, 20090732)+2 种基金Jilin Provincial Development and Reformation Committee(No.2009Y042J12314)Jilin Province Talent Development Foundation (No.JRJB2007-2)the Natural Science Foundation of China(Nos.30670301, 30870354)
文摘Cyclin-dependent kinase 2-associated protein 1（CDK2AP1）, a cell growth inhibitory factor, is abnormally expressed in cancer cells, and might be implicated in the development of lung cancer. However, no studies on the function of CDK2AP1 in human lung cancer have been yet reported. In this study, overexpressing lentiviral vectors containing full-length CDK2AP1 cDNA and CDK2AP1 shRNA（short hairpin RNA） were constructed. Our results show that infecting A549 cells with lentivirus containing CDK2AP1 shRNA or full-length CDK2AP1 cDNA results in significantly down- or up-regulated the expression of CDK2AP1, respectively, thereby providing reliable tools for studying the function of CDK2AP1 in pulmonary carcinogenesis. Our data of MTT assay and flowcytometric analysis demonstrate that CDK2AP1 plays an important role in the proliferation/growth and cell cycling of A549 cells in vitro, and further investigation into its underlying mechanism of pulmonary carcinogenesis is needed.
