PubMed:10077156 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PubMed/sourceid/10077156","sourcedb":"PubMed","sourceid":"10077156","source_url":"http://www.ncbi.nlm.nih.gov/pubmed/10077156","text":"Glucocorticoid hormone suppression of human neutrophil-mediated tumor cell cytostasis.\nIn the present study, we have investigated the effect of glucocorticoid hormones on neutrophil-mediated tumor cell cytostasis and found that hydrocortisone and a synthetic hormone, dexamethasone (Dex), inhibited cytostasis in the presence or absence of tumor necrosis factor-alpha. The effect of Dex was completely reversed by a glucocorticoid receptor antagonist, RU38486. To clarify the underlying mechanisms, we examined effects of Dex on the binding avidity of beta2 integrin on the neutrophil surface and how these might in turn affect neutrophil-to-tumor cell binding. Dex was found to inhibit these neutrophil properties, and RU38486 completely suppressed both forms of Dex inhibition. Taken together, our findings suggest that glucocorticoid hormone inhibition of neutrophil-mediated tumor cell cytostasis is at least partially due to a lowering of the ligand binding avidity of beta2 integrin on the neutrophil 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