Macrophage and Cancer Cell.pdfVIP

get_box_var; ORIGINAL ARTICLE Macrophage and Cancer Cell Cross-talk via CCR2 and CX3CR1 Is a Fundamental Mechanism Driving Lung Cancer 1 1 2 3 4 1 Anja Schmall , Hamza M. Al-tamari , Susanne Herold , Marian Kampschulte , Andreas Weigert , Astrid Wietelmann , 1 2 1,2 1,2 1,2 Natasha Vipotnik , Friedrich Grimminger , Werner Seeger , Soni Savai Pullamsetti , and Rajkumar Savai 1Department of Lung Development and Remodeling, Max Planck Institute for Heart and Lung Research, German Center for Lung Research, Bad Nauheim, Germany; 2Department of Internal Medicine and 3Department of Radiology, Universities of Giessen and Marburg Lung Center, German Center for Lung Research, Justus-Liebig University, Giessen, Germany; and 4Institute of Biochemistry I, Goethe-University Frankfurt, Frankfurt, Germany Abstract migration and MF M2 polarization. In vivo, MF depletion (clodronate, MF Fas-induced apoptosis mice) and genetic ablation Rationale: Recent studies indicate that tumor-associated of CCR2 and CX3CR1 all inhibited LLC1 tumor growth and macrophages (MF) with an M2 phenotype can influence cancer metastasis, shifted tumor-associated MF toward M1 polarization, progression and metastasis, but the regulatory pathways remain suppressed tumor vessel growth, and enhanced survival poorly characterized. (metastasis model). Furthermore, mice treated with CCR2