4.5 Article

CX3CL1 promotes lung cancer cell migration and invasion via the Src/focal adhesion kinase signaling pathway

Journal

ONCOLOGY REPORTS
Volume 41, Issue 3, Pages 1911-1917

Publisher

SPANDIDOS PUBL LTD
DOI: 10.3892/or.2019.6957

Keywords

non-small cell lung cancer; migration; invasion; Src; focal adhesion kinase; saracatinib

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Funding

  1. National Natural Science Foundation of China [81572629]

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The present study investigated the role of C-X3-C motif chemokine ligand 1 (CX3CL1) in lung cancer cell migration and invasion and its potential mechanism. The expression levels of C-X3-C motif chemokine receptor 1 (CX3CR1) in six human lung cancer cell lines and one human bronchial epithelial cell line were assessed using reverse transcription-quantitative polymerase chain reaction and western blotting. Cell proliferation was assessed using the Cell Counting Kit-8 assay. Cell migration and invasion were examined using the Transwell assay, with and without Matrigel, respectively. The signaling pathway activated by CX3CL1 was analyzed via western blotting and inhibitory migration and invasion assays. CX3CR1 was expressed in the six lung cancer cell lines and one normal lung cell line. The lung cancer cell line, H460, was selected for further study. CX3CL1 did not significantly affect H460 proliferation; however, CX3CL1 did significantly enhance the migration and invasion of H460 cells. The Src/focal adhesion kinase (FAK) signaling pathway was activated in a time-dependent manner upon stimulation of CX3CL1. However, blocking Src activity with saracatinib prevented CX3CL1-mediated cell migration and invasion. Therefore, the findings indicated that CX3CL1 promotes lung cancer cell migration and invasion in vitro, and the Src/FAK signaling pathway serves a vital role in this process.

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