Interferon-induced increase in neuraminidase-releasable sialic acid and glycosphingolipid metabolism in mouse lymphoma and l1210 leukemic cell lines: Correlation with susceptibility to natural killer cell-mediated lysis

✍ Scribed by G. Yogeeswaran; A. Grönberg; R. M. Welsh; R. Kiessling

• Publisher: John Wiley and Sons
• Year: 1983
• Tongue: French
• Weight: 744 KB
• Volume: 31
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/ijc.2910310417

✦ Synopsis

Abstract

Changes in sialoglyoconjugates and glycosphingolipid (GSL)^5^ metabolism were demonstrated in mouse EL4, P52 and YAC‐1 lymphoma and L1210 leukemia cell lines treated with β‐interferon (IFN). Expression of cell surface (neuraminidase‐releasable) sialic acid on IFN‐treated cells was markedly elevated (three‐ to six‐fold). The increase in neuraminidase‐releasable sialic acid is contributed by sialoglycoproteins and particularly by cell‐surface gangliosides in IFN‐treated cells. Incorporation of [^3^H]‐galactose into all GSL was elevated in IFN‐treated cells. Thin‐layer chromatographic analysis of GSL of IFN‐treated cells showed an increase in several GSL homologues with striking changes in ganglioside with chromatographic migration of G~M2~, G~M1~, and G^D1a^ relative to control cells. IFN‐treated tumor‐cell lines became resistant to lysis by virus‐induced IFN‐activated natural killer (NK) cells, as shown previously, but addition of neuraminidase to IFN‐treated and untreated cells caused only a moderate increase in NK‐sensitivity. This suggests that IFN‐mediated protection of target cells from NK lysis was not due to a preferential masking of target structure by elevated levels of sialic acid. These membrane‐associated changes in GSL and sialic acid in IFN‐treated cells may be potentially significant, because a correlation between certain GSL expression, sialic acid phenotype and susceptibility of target cells to NK‐cell‐mediated lysis have been found in several other systems.