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Effects of type‐I and ‐II interferons on 90K antigen expression in ovarian carcinoma cells
Author(s) -
Marth Christian,
Dreps Andreas,
Natoli Clara,
Zeimet Alain G.,
Lang Thomas,
Widschwendter Martin,
Daxenbichler Günter,
Ullrich Axel,
Iacobelli Stefano
Publication year - 1994
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.2910590617
Subject(s) - interferon , biology , lymphokine , antigen , secretion , cancer research , ovarian carcinoma , interferon gamma , cell culture , messenger rna , ovarian cancer , immunology , microbiology and biotechnology , cytokine , cancer , endocrinology , biochemistry , gene , genetics
Antigen 90K is produced by several tumor‐cell lines and by patients with cancer. Its function has not yet been clarified, although recent reports suggest that it plays a role in the tumor—host relationship—for example by stimulation of natural killer and lymphokine‐activated killer‐cell activity. Previous studies have indicated that 90K expression may be under the influence of interferon‐α. Here, we provide evidence that both interferon‐α and ‐γ can enhance the secretion of 90K and augment the level of specific mRNA expression in 3 ovarian carcinoma cell lines (OVCAR‐3, HTB‐77 and SKOV‐6). However, interferon‐γ leads to depletion of cellular 90K whereas interferon‐α increases both secreted and cellular 90K levels. In equimolar concentrations, Interferon‐α was always superior to interferon‐γ in augmenting 90K protein or mRNA levels. Combinations of TNF with interferon‐γ were highly synergistic both in reducing cell proliferation and in increasing 90K secretion and mRNA expression. This synergism was seen to a lesser extent with interferon‐α.