Presenters: Sanyah Garcia-Nava ; Rosa Flores
Authors: Sanyah Garcia-Nava, Rosa Flores, Cassandra Finkbeiner, Richard Warner
Faculty Advisor: Richard Warner
Institution: Dixie State University
Recently, treatments for melanoma cancer patients have been focusing on immune checkpoint blockade, which allows for T-cells to be reactivated to fight tumor growth. These treatments have improved survival outcomes of melanoma patients, but there is a need for further research of immune signaling in melanoma to understand possibilities for additional therapy targets. The goal of our research project is to study the interaction of B7-H3, an immune signaling protein that is overexpressed in cancers including melanoma, and midkine, a heparin-binding growth factor, which has an important role in the replication, development, and repair of cells, and is involved in the progression of cancer malignancies as well. Both molecules are candidates for potential cancer immunotherapy as mediators of B7-H3 immune checkpoint signaling or similar potential role in regulation of the immune response. For our research of midkine and B7-H3 protein activities we are using an immortalized line of human T-lymphocyte cells, known as Jurkat cells, to analyze the interaction by co-immunoprecipitation from a cellular setting similar to their biological localization in melanomas. Currently, we have grown Jurkat cells in RPMI 1640 medium and activated them with PMA and Ionomycin. In the activated state, we see greater binding of purified B7-H3 protein to the Jurkat cells. We collected lysates from either inactive or activated states to confirm their detection by co-immunoprecipitation followed with western blot analysis. Next, we hope to examine the effect of this interaction on B7-H3 immune signaling and also toward growth signaling induced by midkine in the Jurkat cells. This research will provide insight into cancer resistance mechanisms and the potential for therapy based on B7-H3 or midkine to bring additional options to cancer patients.