Nasal natural killer/T-cell lymphoma (NNKTL) is associated with the Epstein-Barr virus (EBV), and has distinct histological features such as angiocentric and polymorphous lymphoreticular infiltrates that contain too many cell types, including tumour and inflammatory cells. We have previously shown that intercellular adhesion molecule (ICAM)-1 is expressed in NNKTL cells, and that soluble ICAM-1 (sICAM-1) is significantly increased in patients’ sera. However, the functional role of sICAM-1 remains unknown. In the present study, we found that EBV-positive NNKTL cell line SNK6 secreted sICAM-1 in a time-dependent manner. Moreover, exogenous sICAM-1 enhanced the growth of SNK6 cells in a dose-dependent manner. Comparatively, neutralising ICAM-1 and LFA-1 antibodies, as well as the LFA-1 blocker simvastatin, caused a dose-dependent reduction in the number of viable SNK6 cells. Double immunohistological staining of NNKTL tissues confirmed that CD56 positive lymphoma cells co-expressed LFA-1. Moreover, serum sICAM-1 levels in NNKTL patients decreased after treatment, suggesting that the levels reflected disease progression. We conclude that NNKTL cells secrete sICAM-1 that acts as an autocrine factor for lymphoma progression, and suggest that simvastatin may be a potential candidate to treat NNKTL.
