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Published 5 January 2004. doi:10.1083/jcb.200310041
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 164, Number 1, 89-96
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Article

Apaf-1 and caspase-9 do not act as tumor suppressors in myc-induced lymphomagenesis or mouse embryo fibroblast transformation



Clare L. Scott1, Martin Schuler2, Vanessa S. Marsden1, Alex Egle1, Marc Pellegrini1, Dobrila Nesic1, Steve Gerondakis1, Stephen L. Nutt1, Douglas R. Green2 and Andreas Strasser1

1 The Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria, 3050, Australia
2 La Jolla Institute for Allergy and Immunology, San Diego, CA 92121

Address correspondence to Andreas Strasser, The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria, 3050 Australia. Tel.: 61-3-9345-2464 Fax: 61-3-9347-0852. email: strasser{at}wehi.edu.au

Based on experiments with cultured fibroblasts, the apoptosis regulators caspase-9 and Apaf-1 are hypothesized to function as tumor suppressors. To investigate their in vivo role in lymphomagenesis, an IgH enhancer-driven c-myc transgene was crossed onto Apaf-1-/- and caspase-9-/- mice. Due to perinatal lethality, Eµ-myc transgenic Apaf-1-/- or caspase-9-/- fetal liver cells were used to reconstitute lethally irradiated recipient mice. Surprisingly, no differences were seen in rate, incidence, or severity of lymphoma with loss of Apaf-1 or caspase-9, and Apaf-1 was not a critical determinant of anticancer drug sensitivity of c-myc–induced lymphomas. Moreover, loss of Apaf-1 did not promote oncogene-induced transformation of mouse embryo fibroblasts. Thus, Apaf-1 and caspase-9 do not suppress c-myc–induced lymphomagenesis and embryo fibroblast transformation.

Key Words: apoptosis; cancer; Bcl-2; Apaf-1; caspase

M. Schuler and V.S. Marsden contributed equally to this work.

The online version of this article contains supplemental material.

C. Scott's present address is Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724.

M. Schuler's present address is Johannes Gutenberg University Hospital, Mainz, 55101, Germany.

A. Egle's present address is University Hospital Innsbruck, Laboratory for Molecular Cytology, Innsbruck, 6020, Austria.

D. Nesic's present address is Institute of Pathology, University of Bern, Bern, 3010, Switzerland.

Abbreviations used in this paper: C9DN, caspase-9 dominant-negative; MEF, mouse embryo fibroblast; PI, propidium iodide.


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