290802 Role of Wisp-1 in the Suppression of Interleukin-12 Signaling in Immune Cells

Monday, October 29, 2012
Hall B (Convention Center )
Nathan Mickinac, Emily Chambers and David Klinke, Chemical Engineering, West Virginia University, Morgantown, WV

An emerging hallmark of cancer is that malignant cells suppress anti-tumor immunity. Host immunity is a complex process that is regulated by secreted biochemical cues (cytokines). One key cytokine that regulates cytotoxic immunity is Interleukin-12 (IL12). We have previously observed that melanoma cells secrete biochemical cues that suppress the cellular response to IL12. One of the proteins secreted by melanoma cells, as modeled by the B16 cell line, is WNT1-inducible-signaling pathway protein 1 (WISP-1). WISP-1 is a member a family of growth factors that has several effects on tumor growth and tissue development. We hypothesize that WISP-1 suppresses the response of an immune cell model (2D6 cells) to IL12. Our approach to test this hypothesis was to knock down the production of WISP-1 via transfecting siRNA  and to assess the impact of WISP-1 expression on a co-culture of 2D6 with B16 cells. On-going results will be discussed, which focus on determining the initial levels of WISP-1 present in B16 cells within the co-culture assay.

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