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Decreased expression of ICAM-1 and its induction by tumor necrosis factor on breast-cancer cells in vitro

✍ Scribed by Alexandra C. Budinsky; Thomas Brodowicz; Christoph Wiltschke; Klaus Czerwenka; Ilse Michl; Michael Krainer; Christoph C. Zielinski

Publisher: John Wiley and Sons
Year: 1997
Tongue: French
Weight: 53 KB
Volume: 71
Category: Article
ISSN: 0020-7136
DOI: 10.1002/(sici)1097-0215(19970611)71:6<1086::aid-ijc27>3.0.co;2-a

No coin nor oath required. For personal study only.

✦ Synopsis

In order to study adhesion-molecule expression and its consequences for cellular recognition, the presence of adhesion molecules ICAM-1, VCAM-1, VLA-4, LFA-1, alpha, LFA-1 beta, LFA-3, b1-integrin and b3-integrin was studied on specimens from breast tissue by immunohistochemistry and on cells from breast cell lines propagated in vitro. Breastcancer tissue and the breast-cancer cell lines MCF-7, SK-BR-3 and ZR-75-1 showed expression of ICAM-1 and VLA-4 significantly lower than that of benign breast cells or normal breast epithelium. Of various cytokines tested, including recombinant human (rh) interleukin-6 (IL-6), rh tumor necrosis factor alpha (TNF-a), interleukin 2 (IL-2), granulocyte/macrophagecolony-stimulating-factor (GM-CSF), interferon-alpha (IFN-a) and interferon-gamma (IFN-g), only TNF was able to reinduce expression of ICAM-1 on cells from MCF-7, SK-BR-3 and ZR-75-1. Further, the ability of either unstimulated or lymphokine-stimulated killer (LAK) cells to recognize and lyse native or TNF-stimulated breast-cancer cells was studied. Whereas neither unstimulated lymphocytes or LAK cells were able to lyse untreated breast-cancer cells deficient for ICAM-1 expression, pre-treatment of tumor cells with TNF led to increased tumor-cell lysis. Anti-ICAM-1 antibodies, and pre-treatment of tumor cells with anti-TNF-receptor antibodies, abrogated these findings, corroborating their specificity. We thus conclude that the defective expression of ICAM-1 in our model might constitute a mechanism by which breastcancer cells escape immunologic recognition and lysis by appropriate effector cells.

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