Journal: Oncogene
Article Title: Copy number variations of HLA-I and activation of NKp30 pathway determine the sensitivity of gastric cancer cells to the cytotoxicity of natural killer cells
doi: 10.1038/onc.2015.324
Figure Lengend Snippet: Schematic representation of the proposed mechanism of NK cell lysis for cancer cells. Two human GC cell lines, AGS and BGC823, were used in this study. As left shown, AGS cells did not express HLA-C due to the loss of DNA copy, and NK cells were activated because of active NKp30/VAV2/MAPK3/IL-12 pathway in AGS cells. As right shown, BGC823 cells highly expressed HLA-I, an inhibitor of NK cell recognition, due to gene amplification, and NK cells were not activated because of lacking NKp30 in BGC823 cells.
Article Snippet: We used antibodies against HLA-A (1913–1; Epitomics, Burlingame, CA, USA), HLA-B (2389–1; Epitomics), HLA-C (5472–1; Epitomics), MICA (T3305; Epitomics), VAV2 (B1241; Anbo, San Francisco, CA, USA), MAPK3 (C11133; Anbo), NKp30 (BS3888; Bioworld, St Louis Park, MN, USA), and pERK (Tyr204) (sc-7383; Santa Cruz Biotechnology, Santa Cruz, CA, USA), Bag6 (6763–1; Epitomics) and actin (A5441; Sigma, St Louis, MO, USA).
Techniques: Lysis, Amplification