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Category:Patronymic surnamesPro-inflammatory cytokines, including interleukin-6 (IL-6), can have both pro- and anti-neoplastic properties in cancer. IL-6 stimulates the production of hepatocyte growth factor (HGF) and its receptor, c-Met, which can promote cell growth, migration, and invasion in some cancers. We have found that IL-6 stimulates both HGF production in tumor cells and c-Met signaling in stromal cells of the tumor microenvironment (TME). Since it is thought that resistance to anti-VEGF treatments is mediated by the c-Met pathway, we wanted to further investigate c-Met in the TME. We hypothesized that the anti-inflammatory cytokine IL-10 stimulates the production of the secreted form of IL-6, IL-6S, that then stimulates the production of HGF and c-Met in tumor cells, leading to increased resistance to anti-VEGF drugs. Using murine tumor xenograft models, we have found that IL-6S is increased in tumors after treatment with anti-VEGF drugs and is increased further in tumors after IL-6/IL-6R blockade. Using genetic and pharmacological approaches, we have found that IL-6/IL-6R signaling in stromal cells of the TME is important for tumor development and growth, as well as resistance to anti-VEGF treatments. Our most recent experiments have shown that IL-6/IL-6R signaling in stromal cells leads to the activation of STAT3 and AKT in tumor cells, and that IL-6/STAT3/AKT-mediated resistance to anti-VEGF drugs requires HGF production by tumor cells. We are currently working to identify the mechanisms whereby stromal cells promote IL-6S production, and to identify the inflammatory cytokines other than IL-6 that lead to increased IL-6S. These studies are important for our understanding of tumor development, progression, and resistance to anti-VEGF treatments. In addition to testing our hypothesis, we are also using immunofluorescence, FACS, MTT, and xenograft studies to determine the roles of cell intrinsic versus cell extrinsic signaling pathways in mediating IL-6S and c-Met. In this project, we will test the following hypotheses: Hypothesis 1: IL-
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