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Analysis of differentially expressed genes between the high-metastatic and low-metastatic lung cancer cell lines  期刊论文  

  • 编号:
    d8766527-8ff7-4831-9bf2-1ca658b6a723
  • 作者:
    Li, Jing[0][1] Lin, Hechun[1][2] Zhang, Fanglin[2][3] Yu, Jingxian[3][4] Sa, BingQing[4][5] Liu, Lei[5][6] Yan, Mingxia[6][2] Yao, Ming[7][2]
  • 地址:

    [1]s Republic of China, Zhejiang Provincial Key Laboratory of Plant Virology,Beijing,China

    [2]Renji Hospital, State Key Laboratory of Oncogenes and Related Genes,Shanghai,China

    [3]Fudan University Shanghai Medical College,Shanghai,China

    [4]University of Adelaide, School of Physical Sciences,Adelaide,Australia

    [5]Shanghai Jiao Tong University School of Medicine, State Key Laboratory of Oncogenes and Related Genes,Shanghai,China

    [6]China Academy of Engineering Physics, Research Center of Laser Fusion,Chengdu,China

  • 语种:
    中文
  • 期刊:
    Tumor ISSN:1000-7431 2012 年 32 卷 3 期 (164 - 169)
  • 收录:
  • 关键词:
  • 摘要:

    Objective: To analyze the metastatic mechanism and its related molecular signaling pathways in the high-metastatic human lung cancer cell line SPC-A-1sci as compared with the low-metastatic human lung cancer cell line SPC-A-1 as the control, and to find the key genes for lung cancer metastasis. Methods: The differentially expressed genes between the high-metastatic human lung cancer cell line SPC-A-1sci and the low-metastatic human lung cancer cell line SPC-A-1 were detected by microarray. The potential key genes and the related signal pathways in lung cancer metastasis were examined by bioinformatics analyses including pathway analyses and signal transduction networks. Results: As compared with the SPC-A-1 cells, 2 892 genes were up-regulated and 3 248 genes were down-regulated in the SPC-A-1sci cells. There were 48 signal transduction pathways involved in the up-regulated genes and 65 signal transduction pathways involved in the down-regulated genes. The key genes in the signal transduction networks were mitogen-activated protein kinase-1, epidermal growth factor receptor, AKT 1, AKT 3, phosphoinositide-3-kinase, catalytic, delta polypeptide (PIK 3CD ), phosphoinositide-3-kinase 3, regulatory subunit1 (alpha) (PIK 3R 1), PIK 3R 3, KRAS , and insulin-like growth factor-1 receptor. Conclusion: The applications of gene chip technology and bioinformatics tools in the investigation of metastatic mechanism and its related molecular signaling pathways of high-metastatic lung cancer cell line SPC-A-1sci provide evidences for the basic research and the clinical prevention and treatment research for lung cancer metastasis. Copyright© 2012 by TUMOR.

  • 推荐引用方式
    GB/T 7714:
    Li Jing/26643007400[0],Lin Hechun/56010292000[1],Zhang Fanglin/55788400600[2], 等. Analysis of differentially expressed genes between the high-metastatic and low-metastatic lung cancer cell lines [J].Tumor,2012,32(3):164-169.
  • APA:
    Li Jing/26643007400[0],Lin Hechun/56010292000[1],Zhang Fanglin/55788400600[2],Yu Jingxian/15063744800[3],&Yao Ming/56579620100[7].(2012).Analysis of differentially expressed genes between the high-metastatic and low-metastatic lung cancer cell lines .Tumor,32(3):164-169.
  • MLA:
    Li Jing/26643007400[0], et al. "Analysis of differentially expressed genes between the high-metastatic and low-metastatic lung cancer cell lines" .Tumor 32,3(2012):164-169.
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