ABSTRACTS â ORAL PRESENTATIONS - AMCA, spol. s r.o.

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200 cGy and fixed 30 min after irradiation for measurements using flow cytometry. Sectors Q3 represent control level of γH2AX, sectors Q4 contain cells with increased γH2AX intensity. γH2AX signal was measured as FITC intensity (X-values). Y-axis shows side scatter of cells. 58. TUMOR-DRIVEN CHANGES IN HUMAN MESENCHYMAL STROMAL CELLS CAN GENERATE PHENOTYPE OF CARCINOMA-ASSOCIATED FIBROBLASTS Lucia Kucerova 1 , Jakub Zmajkovic 2 , Lenka Baranovicova 1 , Svetlana Skolekova 1 , Miroslava Matuskova 1 1 Laboratory of Molecular Oncology, Cancer Research Institute, Slovak Academy of Sciences, Vlarska 7, 833 91 Bratislava, Slovak Republic, lucia.kucerova@savba.sk 2 Arsanis Biosciences GmbH, Helmut-Qualtinger-Gasse 2, 1030 Vienna, Austria Background: Human mesenchymal stromal cells have been added to the list of numerous non-malignant cells contributing to tumor microenvironment thereby influencing tumor growth and progression. Tumor-produced paracrine factors are capable of driving molecular changes leading towards the differentiation of MSC into cells with the properties of carcinoma associated fibroblasts. MSC interaction with particular tumor cells is either tumor supportive or suppressive, and the underlying mechanisms remain to be elucidated [1-3]. We hypothesize that it is the tumor-dictated process of molecular changes in MSC responsible for the tumor growth support/inhibition. Methods: Project should unravel effects of tumor produced paracrine factors on MSC properties, such as differentiation capacity, immunophenotype and cytokine expression profile. More importantly, changes in production of proteins affecting tumor vascularization, aggressiveness, invasiveness and other sequence of events leading toward acquired carcinoma associated fibroblast phenotype in MSC dictated by tumor microenvironment were evaluated. These events were mimicked by long-term culture of MSC under the influence tumor-derived paracrine factors in vitro. Moreover, these Analytical Cytometry VII 73
effects will be also characterized upon MSC coimplantation with the tumor cells in vivo in the future. (Fig. 1). Figure 1. Experimental design and the outcomes to be evaluated in the process of tumor cell-driven MSC differentiation. Results: Our data previously documented both tumor-promoting and tumor-suppressive effects of MSC on different human tumor cells both in vitro and in vivo. Human melanoma cells A375 represented the promoting features and induced expression of VEGFR2, FSP, vimentin, αSMA and endosialin in MSC, which were indicative of differentiation towards carcinoma-associated fibroblasts. Human glioblastoma cells 8-MG-BA represented the inhibitory features and did not upregulate these proteins. On the contrary, paracrine stimulation with these cells led to upregulation of genes involved in adipocyte differentiation leading to the idea, that these cells promote aberrant terminal differentiation of MSC with the tumor-suppressive outcome. Several surface markers characteristic for the MSC were evaluated and multiple changes in CD73, CD90, CD105, CD133, CXCR4, CD166, CD146, BCRPI, HLA-DR, CD44, CD31 and CD34 III were detected. Tumor cells also affected migratory properties of MSC and altered the secretome profile of the treated MSC. Many proinflamatory cytokines were upregulated significantly by incubation in the A375-conditioned medium, including VEGF secretion and VEGFR2 expression. Conclusion: Our data attempted to contribute to the understanding of tumor biology by unraveling mechanisms involved in tumor-driven effects on non-neoplastic stromal cells. 74 Analytical Cytometry VII
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Acknowledgements This work was supp
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ABSTRACTS â ORAL PRESENTATIONS - AMCA, spol. s r.o.