Effect of Neuraminidase on Growth of a 3-Methylcholanthrene-Induced Fibrosarcoma in Normal and Immunosuppressed Syngeneic Mice2

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Abstract
Treatment of a weakly immunogenic 3-methylcholanthrene-induced fibrosarcoma (MC-42) with Vibrio cholerae neuraminidase (VCN) in vitro interfered with growth of the tumor cells in syngeneic C3H/HeJ female mice. Palpable tumors did not appear in some recipients, and many of the tumors which did appear spontaneously regressed. The effect could be detected at all tumor cell doses and at low concentrations of VCN. The recipients that survived were frequently immune to subsequent inoculations of large numbers of MC-42 cells, but tolerated the growth of immunologically distinct, 3-methylcholanthrene-induced fibrosarcomas (MC-43). The inhibitory effect of VCN treatment on tumor growth was abrogated by heat inactivation of the enzyme or by incubation of the enzyme with sialic acid—a negative feedback inhibitor of neuraminidase. VCN-treated tumor cells grew as rapidly as normal cells in immunosuppressed recipients. The results are consistent with the hypothesis that removal of the terminal sialic acid residues from the cell surface does not interfere with the intrinsic growth potential of the tumor cells, but that it increases the immunogenicity of tumor-specific transplantation antigens on the cell surface. Increased tumor immunogenicity is probably the result of changes on the cell surface which make the treated cells more susceptible to immunologic processing by the recipient.

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