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高等学校化学研究 ›› 2011, Vol. 27 ›› Issue (3): 445-449.

• Articles • 上一篇    下一篇

Lentivirus-mediated RNA Interference and Over-expression of CDK2AP1 CDNA Regulate CDK2AP1 Expression in Human Lung Cancer A549 Cells

GAO Nan1, ZHANG Xing-yi1, JIANG Rui2, WANG Guan3, LI Jin-dong1, JIN Cheng-yan1 and SUN Mei4*   

  1. 1. Department of Thoracic Surgery, the Second Hospital of Jilin University, Changchun 130041, R. P. China;
    2. Department of Orthopedic Surgery, China-Japan Union Hospital of Jilin University, Changchun 130033, P. R. China;
    3. Department of Cardiac Medicine, 4. Department of Pathology, the Second Hospital of Jilin University, Changchun 130041, P. R. China
  • 收稿日期:2011-01-18 修回日期:2011-03-25 出版日期:2011-05-25 发布日期:2011-04-29
  • 通讯作者: SUN Mei E-mail:sun.mei55@yahoo.com
  • 基金资助:

    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), Jilin Provincial Development and Reformation Committee(No.2009Y042J12314), Jilin Province Talent Development Foundation (No.JRJB2007-2) and the Natural Science Foundation of China(Nos.30670301, 30870354).

Lentivirus-mediated RNA Interference and Over-expression of CDK2AP1 CDNA Regulate CDK2AP1 Expression in Human Lung Cancer A549 Cells

GAO Nan1, ZHANG Xing-yi1, JIANG Rui2, WANG Guan3, LI Jin-dong1, JIN Cheng-yan1 and SUN Mei4*   

  1. 1. Department of Thoracic Surgery, the Second Hospital of Jilin University, Changchun 130041, R. P. China;
    2. Department of Orthopedic Surgery, China-Japan Union Hospital of Jilin University, Changchun 130033, P. R. China;
    3. Department of Cardiac Medicine, 4. Department of Pathology, the Second Hospital of Jilin University, Changchun 130041, P. R. China
  • Received:2011-01-18 Revised:2011-03-25 Online:2011-05-25 Published:2011-04-29
  • Contact: SUN Mei E-mail:sun.mei55@yahoo.com
  • Supported by:

    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), Jilin Provincial Development and Reformation Committee(No.2009Y042J12314), Jilin Province Talent Development Foundation (No.JRJB2007-2) and the Natural Science Foundation of China(Nos.30670301, 30870354).

摘要: 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.

关键词: Lung, Cancer, CDK2AP1, shRNA, Lentivirus

Abstract: 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.

Key words: Lung, Cancer, CDK2AP1, shRNA, Lentivirus