The transcriptional signature of human ovarian carcinoma macrophages is associated with extracellular matrix reorganization

Florian Finkernagel, Silke Reinartz, Sonja Lieber, Till Adhikary, Annika Wortmann, Nathalie Hoffmann, Tim Bieringer, Andrea Nist, Thorsten Stiewe, Julia M. Jansen, Uwe Wagner, Sabine Müller‐Brüsselbach, Rolf Müller
In: Oncotarget · 2016 · vol. 7(46) , pp. 75339–75352 · doi:10.18632/oncotarget.12180 · PMID:27659538 · PMC5342745 · W2523680188
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Abstract

// Florian Finkernagel 1, * , Silke Reinartz 2, * , Sonja Lieber 1, * , Till Adhikary 1 , Annika Wortmann 1 , Nathalie Hoffmann 1 , Tim Bieringer 1 , Andrea Nist 3 , Thorsten Stiewe 3 , Julia M. Jansen 2 , Uwe Wagner 2 , Sabine Müller-Brüsselbach 1 , Rolf Müller 1 1 Institute of Molecular Biology and Tumor Research (IMT), Center for Tumor Biology and Immunology (ZTI), Philipps University, Marburg, Germany 2 Clinic for Gynecology, Gynecological Oncology and Gynecological Endocrinology, Center for Tumor Biology and Immunology (ZTI), Philipps University, Marburg, Germany 3 Genomics Core Facility, Center for Tumor Biology and Immunology (ZTI), Philipps University, Marburg, Germany * These authors have contributed equally to this work Correspondence to: Rolf Müller, email: [email protected] Keywords: tumor-associated macrophages, resident peritoneal macrophages, macrophage polarization, transcriptional signature, extracellular matrix Received: July 25, 2016      Accepted: September 09, 2016      Published: September 21, 2016 ABSTRACT Macrophages occur as resident cells of fetal origin or as infiltrating blood monocyte-derived cells. Despite the critical role of tumor-associated macrophages (TAMs) in tumor progression, the contribution of these developmentally and functionally distinct macrophage subsets and their alteration by the tumor microenvironment are poorly understood. We have addressed this question by comparing TAMs from human ovarian carcinoma ascites, resident peritoneal macrophages (pMPHs) and monocyte-derived macrophages (MDMs). Our study revealed striking a similarity between TAMs and pMPHs, which was considerably greater that the resemblance of TAMs and MDMs, including their transcriptomes, their inflammation-related activation state, the presence of receptors mediating immune functions and the expression of tumor-promoting mediators. Consistent with these results, TAMs phagocytized bacteria, presented peptide antigens and activated cytotoxic T cells within their pathophysiological environment. These observations support the notion that tumor-promoting properties of TAMs may reflect, at least to some extent, normal features of resident macrophages rather than functions induced by the tumor microenvironment. In spite of these surprising similarities between TAMs and pMPHs, bioinformatic analyses identified a TAM-selective signature of 30 genes that are upregulated relative to both pMPHs and MDMs. The majority of these genes is linked to extracellular matrix (ECM) remodeling, supporting a role for TAMs in cancer cell invasion and ovarian cancer progression.

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