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C. Cheng
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P2.04 - Poster Session/ Biology, Pathology, and Molecular Testing (ID 234)
- Event: WCLC 2015
- Type: Poster
- Track: Biology, Pathology, and Molecular Testing
- Presentations: 1
- Moderators:
- Coordinates: 9/08/2015, 09:30 - 17:00, Exhibit Hall (Hall B+C)
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P2.04-081 - The Role of B7-H4–Expressing Macrophage in Malignant Pleural Effusion (ID 2366)
09:30 - 09:30 | Author(s): C. Cheng
- Abstract
Background:
B7-H4 is a novel protein of the B7 family which regulated tumor immune escape through inhibition of T-cell activation and cytokine secretion. Tumor-associated macrophages (TAM) are a major component of cancer-related inflammation and play a central role in tumor promotion. Previously, some study have shown that B7-H4–expressing macrophage in peripheral blood from lung cancer patients was significantly higher than that from healthy donors and tuberculosis patients. However, the role of B7-H4–expressing macrophage in malignant pleural effusion is unknown.
Methods:
Pleural effusion mononuclear cells (PEMC) were isolated using Histopaque gradient centrifugation. The percentages of B7-H4–expressing CD68[+]cells were estimated by comparing the proportions of labeled cells with respect to total number of CD68[+]cells from the subjects studied. Intracellular staining was performed with FITC-TGF-beta1 mAb through the Cytofix/Cytoperm™ Fixation/Permeabilization Solution Kit. The detection of EMT related proteins by Western blotting and Flow cytometry. Using ROC curve to evaluate the diagnostic values of B7-H4[+]cell percentage in total macrophages in malignant pleural effusion caused by lung cancer.
Results:
In this study, we found that malignant pleural effusion caused by lung cancer have higher level of B7-H4–expressing macrophage than tuberculous pleural effusion, which have diagnostic value for malignant pleural effusion （CD68[+]B7-H4[+] 16.97±10.32%vs 7.17±5.52%，P＜0.01）Further studies indicated that B7-H4–expressing macrophage is a source of TGF-β1, which is the most important factors of epithelial-mesenchymal transition (EMT). As supported, we proved malignant pleural effusion of lung cancer and TGF-β1 can both induce the EMT of A549 cells, accompanying with enhancement of A549 cell migration and invasion ability.
Conclusion:
Taken together, it is suggested that B7-H4–expressing macrophage may promote pleural metastasis of lung cancer though regulate the process of EMT by secreting TGF-β1.
