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Sialomucin and Lytic Susceptibility of Rat Mammary Tumor Ascites Cells¹

Departments of Biochemistry [J. M., S. B., A. P. S.] and Microbiology [C. S., C. E. M.], University of Maine, Orono, Maine 04469

The potential role of cell surface sialomucin in preventing natural killer (NK)-mediated lysis of tumor cell targets has been addressed by comparing the properties of 2 NK-resistant [ascites (ASC) and short-term cultured (STC)] and 2 NK-susceptible [tunicamycin-treated (TUN) and long-term cultured (LTC)] preparations of 13762 MAT-B1 rat mammary tumor cells. Both the ASC and STC cell preparations contain elevated levels of the sialomucin ASGP-1 relative to TUN and LTC preparations as determined by [³H]glucosamine labeling and by binding of peanut agglutinin. The major difference in the susceptibility to NK-mediated lysis appeared to be due to the difference in the susceptibility to lysis by lytic granules, rather than to differences in the ability to bind or trigger effector cells, since TUN and LTC cells were approximately 10-fold more sensitive to lysis by lytic granules than were ASC and STC cells. All preparations inhibited the lysis of the susceptible target YAC-1 by normal rat splenocytes, indicating an ability to bind these effector cells. Triggering of effectors, as monitored either by incorporation of ³²P into phosphatidylinositol or by transmethylation of phosphatidylcholine, was similar for the positive control YAC-1, STC, TUN, and LTC, whereas ASC appeared to be defective in triggering effectors. These results suggest that tumor sialomucin blocks the final phase of lysis, but not the initial recognition of tumor cells by NK effectors.

¹ This work was supported by Grant CA33238 from the NIH [A. P. S.], the Terry Fox Memorial Cancer Research Fund, and Projects 8407 and 8758 from the Maine Life Sciences and Agriculture Experiment Station (Publication 1473).

² To whom requests for reprints should be addressed, at Department of Microbiology, Hitchner Hall, University of Maine, Orono, ME 04469.

Received 4/16/90. Accepted 7/24/90.

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