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Regulation of CD95 (APO‐1/ FAS) ligand and receptor expression in squamous‐cell carcinoma by interferon‐γ and cisplatin
Author(s) -
Moers Cordula,
Warskulat Ulrich,
Müschen Markus,
Even Jos,
Niederacher Dieter,
Josien Régis,
Koldovsky Ursula,
Beckmann Matthias W.,
Häussinger Dieter
Publication year - 1999
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/(sici)1097-0215(19990209)80:4<564::aid-ijc14>3.0.co;2-x
Subject(s) - cisplatin , fas receptor , cancer research , apoptosis , fas ligand , cell culture , biology , receptor , interferon , microbiology and biotechnology , programmed cell death , immunology , chemotherapy , biochemistry , genetics
CD95 (Apo‐1/Fas) ligand (CD95L) expression has been observed in various malignancies. In human primary cell lines from a squamous cell carcinoma (SCC) of the vulva, the effect of cisplatin (CDDP) and IFNγ on the expression of CD95L and its 2 receptor isoforms, CD95 transmembrane (CD95tm) and CD95 soluble receptor, was studied at the mRNA and protein levels. Addition of CDDP and IFNγ increased CD95L mRNA levels in the primary cell line 6‐fold and 1.7‐fold, respectively. In comparison, CD95tm mRNA levels were diminished by CDDP but increased 8‐fold upon IFNγ challenge. CD95L expressed by SCC cells was functionally relevant since these cells were able to induce CD95‐specific apoptosis in autologous lymphocytes from the SCC‐bearing patient. Thus, CD95L expression in SCC may contribute to tumor‐associated immunosuppression, which may be modulated by CDDP and IFNγ. In tumor samples of the primary SCC, CD95L expression was enhanced in the area of the border between invasive tumor tissue and surrounding stroma cells. The locally restricted over‐expression of CD95L was congruent with the arrangement of apoptotic stroma cells in the direct vicinity of invading tumor tongues, suggesting a role as invasion factor for CD95L. Int. J. Cancer 80:564–572, 1999. © 1999 Wiley‐Liss, Inc.