Lung cancer cell invasion and expression of intercellular adhesion molecule-1 (ICAM-1) are attenuated by secretory phospholipase A2 inhibition Jessica.

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Presentation transcript:

Lung cancer cell invasion and expression of intercellular adhesion molecule-1 (ICAM-1) are attenuated by secretory phospholipase A2 inhibition Jessica A. Yu, MD, Miral R. Sadaria, MD, Xianzhong Meng, MD, PhD, Sanchayita Mitra, MS, Lihua Ao, BS, David A. Fullerton, MD, Michael J. Weyant, MD The Journal of Thoracic and Cardiovascular Surgery Volume 143, Issue 2, Pages 405-411 (February 2012) DOI: 10.1016/j.jtcvs.2011.10.026 Copyright © 2012 Terms and Conditions

Figure 1 Intercellular adhesion molecule-1 (ICAM-1) determines invasiveness of lung adenocarcinoma cells. Statistically significant reduction in invasion of A549 cells pretreated with a neutralizing ICAM-1 antibody. ∗P = .003 compared with antibody control, n = 9. The Journal of Thoracic and Cardiovascular Surgery 2012 143, 405-411DOI: (10.1016/j.jtcvs.2011.10.026) Copyright © 2012 Terms and Conditions

Figure 2 Decreased total cellular expression of intercellular adhesion molecule-1 (ICAM-1) in lung adenocarcinoma cells treated with secretory phospholipase A2 (sPLA2) inhibitor. Representative Western blot of A549 cells and H358 cells shows a concentration-dependent decrease in ICAM-1 expression (A). Densitometric analysis of ICAM-1 protein bands normalized to vehicle control. A statistically significant decrease in ICAM-1 expression was seen in both cell lines (B). ∗P < .001 compared with control, n = 4 for each experiment. GAPDH, Glyceraldehyde-3-phosphate. The Journal of Thoracic and Cardiovascular Surgery 2012 143, 405-411DOI: (10.1016/j.jtcvs.2011.10.026) Copyright © 2012 Terms and Conditions

Figure 3 Secretory phospholipase A2 (sPLA2) inhibition of lung adenocarcinoma cells decreases invasion through a modified basement membrane matrix. Representative image of cells that have migrated through the matrix (A). Statistically significant reduction in invasion of A549 cells treated with 20-μmol/L sPLA2 inhibitor for 8 hours (B). ∗P = .019 compared with control, n = 17. The Journal of Thoracic and Cardiovascular Surgery 2012 143, 405-411DOI: (10.1016/j.jtcvs.2011.10.026) Copyright © 2012 Terms and Conditions

Figure 4 Representative immunofluorescent images of group IIa secretory phospholipase A2 (sPLA2) expression in A549 cells. Cell membranes appear green, nuclei appear blue, and sPLA2 appears red. The negative control was cells in vehicle control media and tumor necrosis factor-alpha (TNF-α) for 8 hours stained with non–immune matched immunoglobulin G (A). In the subsequent images, cells were stained with group IIa sPLA2 antibody, vehicle control, and TNF-α for 8 hours (B), TNF-α for 8 hours in the presence of 20-μmol/L sPLA2 inhibitor (C), and TNF-α for 8 hours in the presence of 40-μmol/L sPLA2 inhibitor (D). The decrease in sPLA2 staining was significant at 40-μmol/L sPLA2 inhibitor compared with control (E). ∗P = .023. The Journal of Thoracic and Cardiovascular Surgery 2012 143, 405-411DOI: (10.1016/j.jtcvs.2011.10.026) Copyright © 2012 Terms and Conditions

Figure 5 Group IIa secretory phospholipase A2 (sPLA2) inhibition decreases group IIa sPLA2 production in non–small cell lung cancer cells. Tumor necrosis factor-alpha (TNF-α) for 30 minutes increases production of sPLA2 mRNA (A); ∗P = .022, n = 3 run in triplicate. A 20-μmol/L dose of sPLA2 inhibitor decreases sPLA2 mRNA expression (B); ∗P = .044, n = 3 run in triplicate. The Journal of Thoracic and Cardiovascular Surgery 2012 143, 405-411DOI: (10.1016/j.jtcvs.2011.10.026) Copyright © 2012 Terms and Conditions