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Mechanism of interaction between cisplatin and human recombinant interferon gamma in human ovarian‐cancer cell lines
Author(s) -
Nehmé Alissar,
Albin Nicolas,
Caliaro Marie Josée,
Guichard Sylvie,
Jozan Suzanne,
Julia AnneMarie,
Bugat Roland,
Canal Pierre
Publication year - 1995
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.2910610510
Subject(s) - cisplatin , cell culture , ovarian cancer , interferon gamma , cancer research , recombinant dna , microbiology and biotechnology , biology , glutathione , ovarian carcinoma , chemistry , immunology , cancer , enzyme , gene , biochemistry , cytokine , chemotherapy , genetics
Human ovarian carcinoma cells (2008 and its cisplatin‐resistant sub‐line 2008/C13*) were sensitized to cisplatin by treatment with human recombinant gamma interferon (IFNγ). IFNγ produced no significant change in the uptake of CDDP. Exposure of 2008 and 2008/C13* cells to IFNγ resulted in a time‐dependent decrease of cellular glutathione and total glutathione‐S‐transferase activity, principally the π isoform. By contrast, the treatment of 2008 and 2008/C13* cell lines with IFNγ induced rather than suppressed metallothionein II A mRNA levels. IFNγ changed neither the formation of total platinum‐DNA adducts, nor DNA repair. A significant decrease in c‐ erb B‐2 expression was observed both in sensitive and in resistant cell lines after treatment with IFNγ, and this decrease was dose‐dependent. Our results indicate that the mechanism of IFNγ‐induced sensitization in human ovarian‐cancer cell lines is multifactorial. © 1995 Wiley‐Liss, Inc .

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