CD95 promotes tumour growth
Lina Chen,
Sun-Mi Park,
Alexei V. Tumanov,
Annika Hau,
Kenjiro Sawada,
Christine Feig,
Jerrold R. Turner,
Yang-Xin Fu,
Iris L. Romero,
Ernst Lengyel and
Marcus E. Peter ()
Additional contact information
Lina Chen: The University of Chicago, 924 E 57th Street, Chicago, Illinois 60637, USA
Sun-Mi Park: The University of Chicago, 924 E 57th Street, Chicago, Illinois 60637, USA
Alexei V. Tumanov: The University of Chicago, 5841 South Maryland Avenue, Chicago, Illinois 60637, USA
Annika Hau: The University of Chicago, 924 E 57th Street, Chicago, Illinois 60637, USA
Kenjiro Sawada: The University of Chicago, 5841 South Maryland Avenue, Chicago, Illinois 60637, USA
Christine Feig: The University of Chicago, 924 E 57th Street, Chicago, Illinois 60637, USA
Jerrold R. Turner: The University of Chicago, 5841 South Maryland Avenue, Chicago, Illinois 60637, USA
Yang-Xin Fu: The University of Chicago, 5841 South Maryland Avenue, Chicago, Illinois 60637, USA
Iris L. Romero: The University of Chicago, 5841 South Maryland Avenue, Chicago, Illinois 60637, USA
Ernst Lengyel: The University of Chicago, 5841 South Maryland Avenue, Chicago, Illinois 60637, USA
Marcus E. Peter: The University of Chicago, 924 E 57th Street, Chicago, Illinois 60637, USA
Nature, 2010, vol. 465, issue 7297, 492-496
Abstract:
CD95/Fas promotes tumour growth CD95, known also as Fas and APO-1, is a classical death receptor that regulates tissue homeostasis through apoptosis. Here it is shown that cancer cells, regardless of their sensitivity to CD95-induced apoptosis, depend for optimal growth on CD95. Without CD95 the incidence of ovarian cancer and liver cancer in mice models is reduced, as is their tumour size. CD95 therefore appears to be a double-edged sword: in order to kill tumour cells it may be necessary to reduce, rather than enhance, CD95 activity.
Date: 2010
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Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:465:y:2010:i:7297:d:10.1038_nature09075
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DOI: 10.1038/nature09075
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