Abstract LB-313: Soluble UL16 binding protein 2 is elevated in the sera of lung cancer patients

Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC NKG2D ligands are the surface molecules which induce expression on transformed cells. Specifically they bind to NKG2D on NK cells, and this binding induces activation of NK cells. In humans, NKG2D ligands are described as MICA, MICB and ULBP1, 2, 3, and 4. In this study, we explored the clinical and immunological significance of NKG2D ligands on lung cancer. We evaluated the expression of each NKG2D ligand on the cell surface of various lung cancer cell lines by flow cytometory. The soluble form of ULBP2 was measured in culture supernatant and in sera of lung cancer patients by an original developed ELISA system. Immunological effects of cell surface ULBP2 and soluble form of ULBP2 were examined by 3.5-h 51Cr release assay. We found that ULBP2 was the most widely and strongly expressed NKG2D ligand in lung cancer cell lines. Soluble form of ULBP2 was increased in culture supernatant of the lung cancer cell lines with high expression of cell surface ULBP2. In addition, soluble form of ULBP2 was detectable in the sera of lung cancer patients and increased amount of soluble ULBP2 in sera significantly correlated with poor prognosis lung cancer patients. We evaluated the the immunological effect of soluble ULBP2 separately using human peripheral blood mononuclear cells (PBMCs), and found that soluble ULBP2 suppressed NK activity. In conclusion, ULBP2 is the most significant NKG2D ligand in lung cancer and its soluble form was detectable and elevated in sera of lung cancer patients. Because soluble form of ULBP2 is one of the determinant factor of the anti-tumor immunity of the cancer patients, the development of intervention in this effect would be a candidate for the promising immuno-modulatory therapy Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr LB-313.