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

Yang Chen; Ping Wang

doi:doi:10.11648/j.ajcem.20160404.13

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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

Yang Chen, Ping Wang

Published in American Journal of Clinical and Experimental Medicine (Volume 4, Issue 4)

Received: 16 June 2016 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.

Published in	American Journal of Clinical and Experimental Medicine (Volume 4, Issue 4)
DOI	10.11648/j.ajcem.20160404.13
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), 2016. Published by Science Publishing Group

Keywords

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

References

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APA Style

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://article.sciencepublishinggroup.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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Author Information

Yang Chen

Department of Respiratory Medicine, 306^th Hospital of PLA, Beijing, China
Ping Wang

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

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APA Style

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

Copy | Download

@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://article.sciencepublishinggroup.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}
}

Copy | Download

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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