American Journal of Clinical and Experimental Medicine

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Relationship Between Overexpression of EML4-ALK Variant 1 and Inflammatory Moleculars and Immune Mediators Associated with Tumor Progression and Metastasis in BEAS-2B and H2126 Cells

Received: 16 June 2016    Accepted:     Published: 17 June 2016
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Abstract

The aim of this study was to investigate the relationship between overexpression of EML4-ALK and inflammatory factors about tumor progression and metastasis in a human bronchial epithelial cell (BEAS-2B) and a lung cancer cell (H2126). The recombinant plasmids with EML4-ALK variant 1 and EML4-ALK K589M (EML4-ALK variant 1 kinase inactive mutant) fusion gene were constructed and introduced into H2126 and BEAS-2B cells after transfection. The plasmid pcDNA3.1 was negative control. Subsequent, cell proliferation assay and scratch wound healing assay were used to examine the proliferation and invasion of BEAS-2B and H2126 cells after transfection. Finally, we analyzed 24 inflammatory moleculars and immune mediators associated with tumor progression and metastasis. Compared to the empty vector as control, the expression level of ALK was upregulated in BEAS-2B and H2126 cells after transfection the plasmid EML4-ALK variant 1 and plasmid EML4-ALK K589M. In vitro, EML4-ALK variant 1 promoted the proliferation and invasion ability of BEAS-2B and H2126 cells compared with EML4-ALK K589M and empty vector. The results of Q-PCR showed that factors more differentially expressed between both groups of BEAS-2B and H2126 cells were S100A8 and S100A9 after transfection EML4-ALK variant 1. In conclusion, an increased expression level in S100A8 and S100A9 by overexpression EML4-ALK variant 1 had a great biological interest because of their relation with tumor cell proliferation and migration.

DOI 10.11648/j.ajcem.20160404.13
Published in American Journal of Clinical and Experimental Medicine (Volume 4, Issue 4, July 2016)
Page(s) 103-108
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

EML4-ALK Variant 1, Proliferation, Migration, S100A8, S100A9

References
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Author Information
  • Department of Respiratory Medicine, 306th Hospital of PLA, Beijing, China

  • Department of Respiratory Medicine, 306th Hospital of PLA, Beijing, China

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    Yang Chen, Ping Wang. (2016). Relationship Between Overexpression of EML4-ALK Variant 1 and Inflammatory Moleculars and Immune Mediators Associated with Tumor Progression and Metastasis in BEAS-2B and H2126 Cells. American Journal of Clinical and Experimental Medicine, 4(4), 103-108. https://doi.org/10.11648/j.ajcem.20160404.13

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    ACS Style

    Yang Chen; Ping Wang. Relationship Between Overexpression of EML4-ALK Variant 1 and Inflammatory Moleculars and Immune Mediators Associated with Tumor Progression and Metastasis in BEAS-2B and H2126 Cells. Am. J. Clin. Exp. Med. 2016, 4(4), 103-108. doi: 10.11648/j.ajcem.20160404.13

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    AMA Style

    Yang Chen, Ping Wang. Relationship Between Overexpression of EML4-ALK Variant 1 and Inflammatory Moleculars and Immune Mediators Associated with Tumor Progression and Metastasis in BEAS-2B and H2126 Cells. Am J Clin Exp Med. 2016;4(4):103-108. doi: 10.11648/j.ajcem.20160404.13

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  • @article{10.11648/j.ajcem.20160404.13,
      author = {Yang Chen and Ping Wang},
      title = {Relationship Between Overexpression of EML4-ALK Variant 1 and Inflammatory Moleculars and Immune Mediators Associated with Tumor Progression and Metastasis in BEAS-2B and H2126 Cells},
      journal = {American Journal of Clinical and Experimental Medicine},
      volume = {4},
      number = {4},
      pages = {103-108},
      doi = {10.11648/j.ajcem.20160404.13},
      url = {https://doi.org/10.11648/j.ajcem.20160404.13},
      eprint = {https://download.sciencepg.com/pdf/10.11648.j.ajcem.20160404.13},
      abstract = {The aim of this study was to investigate the relationship between overexpression of EML4-ALK and inflammatory factors about tumor progression and metastasis in a human bronchial epithelial cell (BEAS-2B) and a lung cancer cell (H2126). The recombinant plasmids with EML4-ALK variant 1 and EML4-ALK K589M (EML4-ALK variant 1 kinase inactive mutant) fusion gene were constructed and introduced into H2126 and BEAS-2B cells after transfection. The plasmid pcDNA3.1 was negative control. Subsequent, cell proliferation assay and scratch wound healing assay were used to examine the proliferation and invasion of BEAS-2B and H2126 cells after transfection. Finally, we analyzed 24 inflammatory moleculars and immune mediators associated with tumor progression and metastasis. Compared to the empty vector as control, the expression level of ALK was upregulated in BEAS-2B and H2126 cells after transfection the plasmid EML4-ALK variant 1 and plasmid EML4-ALK K589M. In vitro, EML4-ALK variant 1 promoted the proliferation and invasion ability of BEAS-2B and H2126 cells compared with EML4-ALK K589M and empty vector. The results of Q-PCR showed that factors more differentially expressed between both groups of BEAS-2B and H2126 cells were S100A8 and S100A9 after transfection EML4-ALK variant 1. In conclusion, an increased expression level in S100A8 and S100A9 by overexpression EML4-ALK variant 1 had a great biological interest because of their relation with tumor cell proliferation and migration.},
     year = {2016}
    }
    

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  • TY  - JOUR
    T1  - Relationship Between Overexpression of EML4-ALK Variant 1 and Inflammatory Moleculars and Immune Mediators Associated with Tumor Progression and Metastasis in BEAS-2B and H2126 Cells
    AU  - Yang Chen
    AU  - Ping Wang
    Y1  - 2016/06/17
    PY  - 2016
    N1  - https://doi.org/10.11648/j.ajcem.20160404.13
    DO  - 10.11648/j.ajcem.20160404.13
    T2  - American Journal of Clinical and Experimental Medicine
    JF  - American Journal of Clinical and Experimental Medicine
    JO  - American Journal of Clinical and Experimental Medicine
    SP  - 103
    EP  - 108
    PB  - Science Publishing Group
    SN  - 2330-8133
    UR  - https://doi.org/10.11648/j.ajcem.20160404.13
    AB  - The aim of this study was to investigate the relationship between overexpression of EML4-ALK and inflammatory factors about tumor progression and metastasis in a human bronchial epithelial cell (BEAS-2B) and a lung cancer cell (H2126). The recombinant plasmids with EML4-ALK variant 1 and EML4-ALK K589M (EML4-ALK variant 1 kinase inactive mutant) fusion gene were constructed and introduced into H2126 and BEAS-2B cells after transfection. The plasmid pcDNA3.1 was negative control. Subsequent, cell proliferation assay and scratch wound healing assay were used to examine the proliferation and invasion of BEAS-2B and H2126 cells after transfection. Finally, we analyzed 24 inflammatory moleculars and immune mediators associated with tumor progression and metastasis. Compared to the empty vector as control, the expression level of ALK was upregulated in BEAS-2B and H2126 cells after transfection the plasmid EML4-ALK variant 1 and plasmid EML4-ALK K589M. In vitro, EML4-ALK variant 1 promoted the proliferation and invasion ability of BEAS-2B and H2126 cells compared with EML4-ALK K589M and empty vector. The results of Q-PCR showed that factors more differentially expressed between both groups of BEAS-2B and H2126 cells were S100A8 and S100A9 after transfection EML4-ALK variant 1. In conclusion, an increased expression level in S100A8 and S100A9 by overexpression EML4-ALK variant 1 had a great biological interest because of their relation with tumor cell proliferation and migration.
    VL  - 4
    IS  - 4
    ER  - 

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