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
Volume 4, Issue 4, July 2016, Pages: 103-108
Received: Jun. 16, 2016; Published: Jun. 17, 2016
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Yang Chen, Department of Respiratory Medicine, 306th Hospital of PLA, Beijing, China
Ping Wang, Department of Respiratory Medicine, 306th Hospital of PLA, Beijing, China
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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.
EML4-ALK Variant 1, Proliferation, Migration, S100A8, S100A9
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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, American Journal of Clinical and Experimental Medicine. Vol. 4, No. 4, 2016, pp. 103-108. doi: 10.11648/j.ajcem.20160404.13
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