# These authors contributed equally to this work.
* To whom correspondence should be addressed.
Received September 14, 2016; Revision received October 25, 2016
Overall analysis and understanding of mechanisms are of great importance for treatment of infantile pneumonia due to its high morbidity and mortality worldwide. In this study, we preliminarily explored the function and mechanism of focal adhesion kinase (FAK) in regulation of inflammatory response induced by lipopolysaccharides in A549 cells. Flow cytometry, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, quantitative reverse transcription polymerase chain reaction, and Western blot analysis were used to explore the correlation of FAK expression with cell apoptosis, viability, and the inflammatory cytokine activity in A549 cells. The results showed that knockdown of FAK enhanced cell viability, suppressed apoptosis, and decreased inflammatory cytokine activity. In addition, downregulation of FAK could activate the Wnt and nuclear factor κB signaling pathways. These findings suggest that FAK might be involved in progression of infantile pneumonia and could be a new therapeutic target for this disease.
KEY WORDS: infantile pneumonia, lipopolysaccharides, focal adhesion kinase, Wnt and NF-κB pathways, new therapeutic target