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Slide Presentations: Monday, November 1, 2010 |

Tumor-Associated Macrophages Isolated From Lung Cancer Promote Lung Cancer Cell Invasion FREE TO VIEW

Rui Wang
Author and Funding Information

Center of lung cancer Prevention & Treatment,Shanghai Cancer Hospital, Fudan Uni, Shanghai, Peoples Rep of China



Chest. 2010;138(4_MeetingAbstracts):777A. doi:10.1378/chest.10613
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Abstract

PURPOSE: The aim of our study was to understand whether TAMs from lung cancer tissue can promote lung cancer cells invasion and metastasis, and examine firstly whether invasion and metastasis related cytokines have differential expression in TAMs compared to normal peripheral blood monocytes in primary lung cancer patients.

METHODS: Epidermal Growth Factor(EGF) ,Cathepsin K, cyclooxygenase-2 (COX-2), matrix metalloproteinases -9(MMP-9), Platelet-derived growth factor (PDGF),urokinase-type plasminogen activator(uPA), vascular endothelial growth factor-α (VEGF-α), hepatocyte growth factor(HGF)were evaluated by Real-time PCR. in 53 paired lung cancer patients. Effects of conditioned medium from TAM on different lung cancer cell lines invasion were measured by using Transwell chamber coated with Matrigel.

RESULTS: The expression of Cathepsin K,COX-2,MMP-9,PDGF,uPA,VEGF-α, HGF in TAM were significantly upregulated compared with PBMC. Condition medium from TAM significantly increased cell invasion in SPC-A1(118.6±20.2 and 90.4±13.8, p=0.033), H460(412.4±72.2 and 173±14.7,p=0.000 and A549(363.6±32.4,239.6±19.5,p=0.000).

CONCLUSION: TAM was able to promote lung cancer cell (H460, A549, SPC-A1) invasion(p<0.05), possibly through secreting Cathepsin K,COX-2,MMP-9,PDGF,uPA,VEGF-α, HGF.

CLINICAL IMPLICATIONS: Understanding of mechanisms for TAM-lung cancer cell interactions may lead to identification of new targets for the therapeutic intervention.

DISCLOSURE: Rui Wang, No Financial Disclosure Information; No Product/Research Disclosure Information

4:30 PM - 06:00 PM


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