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Augmentation of Fas ligand-induced apoptosis by MUC1 mucin.

Apoptosis is a physiological mechanism responsible for a wide range of cellular processes during growth, development, carcinogenesis, and inflammation. In this study, we determined whether MUC1 affects Fas ligand (FasL)-induced apoptosis using MUC1 expressing (MUC1(+)) and MUC1(-) cells. Following treatment with 50 nM FasL, apoptosis, caspase-8 activity, and cell surface Fas receptor were measured by cytosolic nucleosome ELISA, colorimetric enzyme assay, and immunofluorescence analysis, respectively. Our results showed that (i) treatment with FasL increased caspase-8 activity (maximum at 4 h) and apoptosis (maximum at 8 h) in both MUC1(+) and MUC1(-) cells, (ii) FasL-induced caspase-8 activity and apoptosis were significantly greater in MUC1(+) cells compared with MUC1(-) cells, (iii) FasL treatment increased cell surface expression of Fas receptor in MUC1(+) cells to a greater extent compared with MUC1(-) cells, (iv) increased cell surface expression of Fas in MUC1(+) cells was not blocked by an inhibitor of protein synthesis (cycloheximide), but was completely abrogated by brefeldin A, an inhibitor of post-translational protein trafficking to the cell surface, and (v) brefeldin A inhibited the increased sensitivity of MUC1(+) cells to FasL-induced apoptosis. We conclude that MUC1(+) cells were more sensitive to FasL-induced apoptosis compared with MUC1(-) cells due to up-regulation of Fas receptor on the cell surface by a mechanism involving increased intracellular trafficking.