Attenuation of focal adhesion kinase reduces lipopolysaccharide-induced inflammation injury through inactivation of the Wnt and NF-κB pathways in A549 cells

Abstract

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.

Integration of Gene Expression Profile Data of Human Epicardial Adipose Tissue from Coronary Artery Disease to Verification of Hub Genes and Pathways

“…In addition, disruption of FAC would also lead to Ado/HC-induced endothelial apoptosis [31] and lipid would deposition following endothelial cell damage. Study also pointed that FAK played a role in reduction of lipopolysaccharide-induced inflammation injury through inactivation of the Wnt and NF-kappaB pathways [32] and inflammation injury was also an important factor during CAD. So focal adhesion signaling might act an important role in vascular endothelial dysfunction and pro-inflammatory reactions, and might be a core change during CAD.…”

RNA-seq profiling reveals differentially expressed genes as potential markers for vital reaction in skin contusion: a pilot study

“…Sfrp2 is considered to be a Wnt antagonist that regulates the Wnt signalling pathway [ 19 ]. Several studies suggest a decrease of Sfrp2 in a variety of cancers; further evidences indicate that Sfrp2 is able to inhibit the Wnt-induced increase in the levels of free β-catenin and influence inflammation and tumour cell proliferation [ 20 , 21 ]. In the present study, Sfrp2 is down-regulated in the contused skin, indicating an activation of Wnt pathway-mediated inflammation.…”

The Crosstalk between FAK and Wnt Signaling Pathways in Cancer and Its Therapeutic Implication

“…A relation between FAK and Wnt signaling was also found in a study evaluating the function and mechanism of FAK in regulating the inflammatory response in the A549 cell line, a model for non-small cell lung cancer (NSCLC). The inhibition of FAK decreased the activation of the Wnt and NF-κB signaling pathways, accompanied by a reduction in inflammatory activity [87]. In another study using the same cell line, FAK was shown to act upstream the Wnt/β-catenin pathway.…”