Effects Of ILK On Production Of Tumor Immune Escape Related Factors Of A549Cells Induced By LPS

Objective:Based on a lung cancer A549cell line stable over-expressing human Integrin-linked kinase (ILK), to explore the effects of ILK on that lung cancer A549cells produce VEGF, TGF-P and IL-6, immune escape related cytokines, induced by Lipopolysaccharide (LPS).Methods:The A549cells line with over-expressing ILK as experimental group was stimulated by LPS, meanwhile, the blank A549cells as control and the saline as negative control factor, then the VEGF, TGF-β and IL-6, immune escape related cytokine, in cell culture lysates and supernatants were determined quantitatively by ELISA respectively and a statistical analysis of the test results were performed too.Results:The independent samples t-test analysis were performed to the quantitative test results VEGF, TGF-P and IL-6. The cell lysates compared with culture supernatants, the three factors had no significant difference (P>0.05); The A549cells line with over-expressing ILK compared with blank A549cells, the three factors were significantly higher (P<0.05); The blank A549cells stimulated by LPS compared with ones stimulated by NS control, there were significant differences in the expression of VEGF, IL-6and TGF-β (P<0.05); The A549cells line with over-expressing ILK stimulated by LPS compared with ones stimulated by LPS, there were significant differences in the expression of VEGF, IL-6and TGF-β; The A549cells line with over-expressing ILK stimulated by LPS compared with blank A549cells stimulated by LPS, the expression of VEGF, TGF-β and IL-6were significantly increased (P<0.05).Conclusion:LPS or ILK over-expression could promote A549cells to produce VEGF, TGF-β and IL-6and the role was more obvious when two factors existed on the cells at the same time. The experimental results show that ILK may play a regulating role in the signaling pathways of promoting tumor effect of pro-inflammatory cytokines.The study laid the foundation to further explore the relationship between ILK, inflammation and tumor, also further confirmed the feasibility that the ILK over-expression A549cell model is applied to the study on the effect and mechanism of ILK.