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Science 2 April 1999:
Vol. 284. no. 5411, pp. 156 - 159
DOI: 10.1126/science.284.5411.156
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Reports

Apaf-1 and Caspase-9 in p53-Dependent Apoptosis and Tumor Inhibition

M. S. Soengas, 1 R. M. Alarcón, 2 H. Yoshida, 3* A. J. , Giaccia, 2 R. Hakem, 3 T. W. Mak, 3 S. W. Lowe 1dagger

The ability of p53 to promote apoptosis in response to mitogenic oncogenes appears to be critical for its tumor suppressor function. Caspase-9 and its cofactor Apaf-1 were found to be essential downstream components of p53 in Myc-induced apoptosis. Like p53 null cells, mouse embryo fibroblast cells deficient in Apaf-1 and caspase-9, and expressing c-Myc, were resistant to apoptotic stimuli that mimic conditions in developing tumors. Inactivation of Apaf-1 or caspase-9 substituted for p53 loss in promoting the oncogenic transformation of Myc-expressing cells. These results imply a role for Apaf-1 and caspase-9 in controlling tumor development.

1 Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.
2 Stanford University School of Medicine, Department of Radiation Oncology, Stanford, CA 94305, USA.
3 Amgen Institute and Ontario Cancer Institute, Department of Medical Biophysics and Immunology, University of Toronto, Toronto, Ontario M5G 2C1, Canada.
*   Present address: Department of Immunology, Medical Institute of Bioregulation, Kyushu University, Fukoka, Japan.

dagger    To whom correspondence should be addressed. E-mail: lowe{at}cshl.org

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J. Cell Biol. 153, 319-328
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Induction of ETS-1 and ETS-2 Transcription Factors Is Required for Thyroid Cell Transformation.
F. de Nigris, T. Mega, N. Berger, M. V. Barone, M. Santoro, G. Viglietto, P. Verde, and A. Fusco (2001)
Cancer Res. 61, 2267-2275
   Abstract »    Full Text »
Tumor Hypoxia: Definitions and Current Clinical, Biologic, and Molecular Aspects.
M. Hockel and P. Vaupel (2001)
J Natl Cancer Inst 93, 266-276
   Abstract »    Full Text »    PDF »
Regulation of p53 by Hypoxia: Dissociation of Transcriptional Repression and Apoptosis from p53-Dependent Transactivation.
C. Koumenis, R. Alarcon, E. Hammond, P. Sutphin, W. Hoffman, M. Murphy, J. Derr, Y. Taya, S. W. Lowe, M. Kastan, et al. (2001)
Mol. Cell. Biol. 21, 1297-1310
   Abstract »    Full Text »
WNT-1 Signaling Inhibits Apoptosis by Activating {beta}-Catenin/T Cell Factor-Mediated Transcription.
S. Chen, D. C. Guttridge, Z. You, Z. Zhang, A. Fribley, M. W. Mayo, J. Kitajewski, and C.-Y. Wang (2001)
J. Cell Biol. 152, 87-96
   Abstract »    Full Text »    PDF »
DNA damage-induced neural precursor cell apoptosis requires p53 and caspase 9 but neither Bax nor caspase 3.
C D'Sa-Eipper, J. Leonard, G Putcha, T. Zheng, R. Flavell, P Rakic, K Kuida, and K. Roth (2001)
Development 128, 137-146
   Abstract »    PDF »
Proteases for Cell Suicide: Functions and Regulation of Caspases.
H. Y. Chang and X. Yang (2000)
Microbiol. Mol. Biol. Rev. 64, 821-846
   Abstract »    Full Text »    PDF »
Bax Is a Transcriptional Target and Mediator of c-Myc-induced Apoptosis.
K. O. Mitchell, M. S. Ricci, T. Miyashita, D. T. Dicker, Z. Jin, J. C. Reed, and W. S. El-Deiry (2000)
Cancer Res. 60, 6318-6325
   Abstract »    Full Text »
Mechanisms of HIV-associated lymphocyte apoptosis.
A. D. Badley, A. A. Pilon, A. Landay, and D. H. Lynch (2000)
Blood 96, 2951-2964
   Abstract »    Full Text »    PDF »
Peg3/Pw1 promotes p53-mediated apoptosis by inducing Bax translocation from cytosol to mitochondria.
Y. Deng and X. Wu (2000)
PNAS 97, 12050-12055
   Abstract »    Full Text »    PDF »
Protein Kinase C Inhibitor and Irradiation-induced Apoptosis: Relevance of the Cytochrome c-mediated Caspase-9 Death Pathway.
S. Rocha, M. S. Soengas, S. W. Lowe, C. Glanzmann, D. Fabbro, K. Winterhalter, S. Bodis, and M. Pruschy (2000)
Cell Growth Differ. 11, 491-499
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Induction of Cell Cycle Progression and Acceleration of Apoptosis Are Two Separable Functions of c-Myc: Transrepression Correlates with Acceleration of Apoptosis.
S. D. Conzen, K. Gottlob, E. S. Kandel, P. Khanduri, A. J. Wagner, M. O'Leary, and N. Hay (2000)
Mol. Cell. Biol. 20, 6008-6018
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Caspase-3 Is Essential for Procaspase-9 Processing and Cisplatin-induced Apoptosis of MCF-7 Breast Cancer Cells.
C. Blanc, Q. L. Deveraux, S. Krajewski, R. U. Jänicke, A. G. Porter, J. C. Reed, R. Jaggi, and A. Marti (2000)
Cancer Res. 60, 4386-4390
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Apoptotic Protease Activating Factor 1 (Apaf-1)-Independent Cell Death Suppression by Bcl-2.
M. Haraguchi, S. Torii, S.-i. Matsuzawa, Z. Xie, S. Kitada, S. Krajewski, H. Yoshida, T. W. Mak, and J. C. Reed (2000)
J. Exp. Med. 191, 1709-1720
   Abstract »    Full Text »    PDF »
Noxa, a BH3-Only Member of the Bcl-2 Family and Candidate Mediator of p53-Induced Apoptosis.
E. Oda, R. Ohki, H. Murasawa, J. Nemoto, T. Shibue, T. Yamashita, T. Tokino, T. Taniguchi, and N. Tanaka (2000)
Science 288, 1053-1058
   Abstract »    Full Text »
Characterization of Calcium Release-activated Apoptosis of LNCaP Prostate Cancer Cells.
I. E. Wertz and V. M. Dixit (2000)
J. Biol. Chem. 275, 11470-11477
   Abstract »    Full Text »    PDF »
p53 Induces Apoptosis by Caspase Activation through Mitochondrial Cytochrome c Release.
M. Schuler, E. Bossy-Wetzel, J. C. Goldstein, P. Fitzgerald, and D. R. Green (2000)
J. Biol. Chem. 275, 7337-7342
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PERP, an apoptosis-associated target of p53, is a novel member of the PMP-22/gas3 family.
L. D. Attardi, E. E. Reczek, C. Cosmas, E. G. Demicco, M. E. McCurrach, S. W. Lowe, and T. Jacks (2000)
Genes & Dev. 14, 704-718
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Apoptosis in cancer.
S. W. Lowe and A. W. Lin (2000)
Carcinogenesis 21, 485-495
   Abstract »    Full Text »    PDF »
CD95 (Fas/APO-1) and p53 Signal Apoptosis Independently in Diverse Cell Types.
L. O’Connor, A. W. Harris, and A. Strasser (2000)
Cancer Res. 60, 1217-1220
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The Role of Apaf-1, Caspase-9, and Bid Proteins in Etoposide- or Paclitaxel-induced Mitochondrial Events during Apoptosis.
C. L. Perkins, G. Fang, C. N. Kim, and K. N. Bhalla (2000)
Cancer Res. 60, 1645-1653
   Abstract »    Full Text »


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