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Association of adriamycin‐induced resistance to NK‐mediated lysis with sialic acid level and immunological reactivity of transferrin receptors and glycophorin A
Author(s) -
Benoist Hervé,
Madoulet Claudie,
Trentesaux Chantal,
Carpentier Yves,
Joly Philippe,
Jardillier Jean Claude,
Desplaces Andrée
Publication year - 1988
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910420227
Subject(s) - neuraminidase , sialic acid , lysis , glycophorin , transferrin receptor , receptor , cytolysis , chemistry , monoclonal antibody , antibody , biology , microbiology and biotechnology , antigen , immunology , biochemistry , cytotoxicity , enzyme , in vitro
Adriamycin (ADM) can increase sialic acid content in K 562 cells and reduce their susceptibility to NK‐mediated lysis. In this report, hypothetical relationship between this resistance and augmentation in sialylation has been investigated. Variations in the time of exposure to ADM showed that 12 hours were sufficient to cause maximal recruitment of benzidinepositive cells, growth inhibition and resistance to NK‐mediated lysis. On the contrary, the membrane sialic acid density seemed stable and 24 hours of drug exposure were necessary to observe a clear rise in sialic acid. Neuraminidase treatment of control and ADM‐treated K 562 cells was associated with an obvious enhancement in their susceptibility to NK‐mediated lysis which can be explained by an increase in the target‐effector binding ability as assessed by a direct conjugate‐forming cell assay. However, the neuraminidase treatment did not modify the sensitivity difference to lysis between untreated and ADM‐treated cells. As compared to control the reactivity of ADM‐treated cells was higher with an antiglycophorin A (GPA) MAb and lower with an antitransferrin receptor (TFR) MAb. Kinetic studies suggested that GPA expression is a better index of ADM‐induced resistance to NK‐mediated lysis than TFR expression. In addition, neuraminidase treatment showed that TFR and GPA modulations induced by ADM can be correlated with sialylation alterations.