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Wild-type p53 can inhibit oncogene-mediated focus formation.
Open accessAbstract
Mutant forms of the p53 cellular tumor antigen elicit neoplastic transformation in vitro. Recent evidence indicated that loss of normal p53 expression is a frequent event in certain types of tumors, raising the possibility that such loss provides transformed cells with a selective growth advantage. Thus, it was conceivable that the mutants might contribute to transformation by abrogating normal p53 function. We therefore studied the effect of plasmids encoding wild-type (wt) p53 on the ability of primary rat embryo fibroblasts to be transformed by a combination of mutant p53 and ras. It was found that wt p53 plasmids indeed caused a marked reduction in the number of transformed foci. Furthermore, wt p53 plasmids also suppressed the induction of transformed foci by combinations of bona fide oncogenes, such as myc plus ras or adenovirus E1A plus ras. On the other hand, plasmids carrying mutations in the p53 coding region totally failed to inhibit oncogene-mediated focus induction and often even slightly stimulated it. Hence, such mutations completely abolished the activity of wt p53 that is responsible for the "suppressor" effect. The latter fact is of special interest, since similar mutations in p53 are often observed in human and rodent tumors. The inhibitory effect of p53 was most pronounced when early-passage cells were used as targets, whereas established cell lines were less sensitive. These data support the notions that wt p53 expression may be restrictive to neoplastic progression and that p53 inactivation may play a crucial role in tumorigenesis.
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Cites
Tumorigenic conversion of primary embryo fibroblasts requires at least two cooperating oncogenes
Land, H., Parada, L. F., & Weinberg, R. A. (1983) · Nature · doi:10.1038/304596a0 · Cited by 2,804
The p53 proto-oncogene can act as a suppressor of transformation
Finlay, C. A., Hinds, P. W., & Levine, A. J. (1989) · Cell · doi:10.1016/0092-8674(89)90045-7 · Cited by 1,987
Ruley, H. E. (1983) · Nature · doi:10.1038/304602a0 · Cited by 1,248
Cited by
A genetic model for colorectal tumorigenesis
Fearon, E. R., & Vogelstein, B. (1990) · Cell · doi:10.1016/0092-8674(90)90186-i · Cited by 12,132
p53 Mutations in Human Cancers
Hollstein, M., Sidransky, D., Vogelstein, B., & Harris, C. C. (1991) · Science · doi:10.1126/science.1905840 · Cited by 8,018
Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Donehower, L. A., Harvey, M., Slagle, B. L., McArthur, M. J., Montgomery, C. A., Butel, J. S., & Bradley, A. (1992) · Nature · doi:10.1038/356215a0 · Cited by 4,649
The E6 oncoprotein encoded by human papillomavirus types 16 and 18 promotes the degradation of p53
Scheffner, M., Werness, B. A., Huibregtse, J. M., Levine, A. J., & Howley, P. M. (1990) · Cell · doi:10.1016/0092-8674(90)90409-8 · Cited by 3,995
Germ Line p53 Mutations in a Familial Syndrome of Breast Cancer, Sarcomas, and Other Neoplasms
Malkin, D., Li, F. P., Strong, L. C., Fraumeni, J. F., Nelson, C. E., Kim, D. H., Kassel, J., Gryka, M. A., Bischoff, F. Z., Tainsky, M. A., et al. (1990) · Science · doi:10.1126/science.1978757 · Cited by 3,765
Momand, J., Zambetti, G. P., Olson, D. C., George, D., & Levine, A. J. (1992) · Cell · doi:10.1016/0092-8674(92)90644-r · Cited by 3,113
Crystal Structure of a p53 Tumor Suppressor-DNA Complex: Understanding Tumorigenic Mutations
Cho, Y., Gorina, S., Jeffrey, P. D., & Pavletich, N. P. (1994) · Science · doi:10.1126/science.8023157 · Cited by 2,551
The first 30 years of p53: growing ever more complex.
Levine, A. J., & Oren, M. (2009) · Nature Reviews Cancer · doi:10.1038/nrc2723 · Cited by 1,967
Self-citationPomerantz, J., Schreiber-Agus, N., Liégeois, N. J., Silverman, A., Alland, L., Chin, L., Potes, J., Chen, K., Orlow, I., Lee, H.-W., et al. (1998) · Cell · doi:10.1016/s0092-8674(00)81400-2 · Cited by 1,521
How does p53 induce apoptosis and how does this relate to p53-mediated tumour suppression
Aubrey, B. J., Kelly, G. L., Janic, A., Herold, M. J., & Strasser, A. (2018) · Cell Death & Differentiation · doi:10.1038/cdd.2017.169 · Cited by 1,395
p53 Activates the CD95 (APO-1/Fas) Gene in Response to DNA Damage by Anticancer Drugs
Müller, M., Wilder, S., Bannasch, D., Israeli, D., Lehlbach, K., Li-Weber, M., Friedman, S. L., Galle, P. R., Stremmel, W., Oren, M., et al. (1998) · The Journal of Experimental Medicine · doi:10.1084/jem.188.11.2033 · Cited by 878
Self-citationTherapeutic targeting of p53: all mutants are equal, but some mutants are more equal than others
Sabapathy, K., & Lane, D. P. (2018) · Nature Reviews Clinical Oncology · doi:10.1038/nrclinonc.2017.151 · Cited by 517
Ben-David, Y., Giddens, E. B., Letwin, K., & Bernstein, A. (1991) · Genes & Development · doi:10.1101/gad.5.6.908 · Cited by 403
Sex Differences in Cancer: Epidemiology, Genetics and Therapy
Kim, H.-I., Lim, H., & Moon, A. (2018) · Biomolecules & Therapeutics · doi:10.4062/biomolther.2018.103 · Cited by 315
The mdm-2 oncogene can overcome wild-type p53 suppression of transformed cell growth.
Finlay, C. A. (1993) · Molecular and Cellular Biology · doi:10.1128/mcb.13.1.301 · Cited by 311
Regulation of the Human hsp70 Promoter by p53
Agoff, S. N., Hou, J., Linzer, D. I., & Wu, B. (1993) · Science · doi:10.1126/science.8418500 · Cited by 292
A functional p53-responsive intronic promoter is contained within the human mdm2 gene
Zauberman, A., Flusberg, D., Haupt, Y., Barak, Y., & Oren, M. (1995) · Nucleic Acids Research · doi:10.1093/nar/23.14.2584 · Cited by 276
Self-citationLin, D., Shields, M. T., Ullrich, S. J., Appella, E., & Mercer, W. E. (1992) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.89.19.9210 · Cited by 267
p53 is frequently mutated in Burkitt's lymphoma cell lines
Farrell, P. J., Allan, G. J., Shanahan, F., Vousden, K. H., & Crook, T. (1991) · The EMBO Journal · doi:10.1002/j.1460-2075.1991.tb07837.x · Cited by 254
Huibregtse, J. M., Scheffner, M., & Howley, P. M. (1993) · Molecular and Cellular Biology · doi:10.1128/mcb.13.2.775 · Cited by 233
Huibregtse, J. M., Scheffner, M., & Howley, P. M. (1993) · Molecular and Cellular Biology · doi:10.1128/mcb.13.8.4918 · Cited by 182
The many faces of p53: something for everyone
Levine, A. J. (2019) · Journal of Molecular Cell Biology · doi:10.1093/jmcb/mjz026 · Cited by 163
p53 Mutations in sporadic adrenocortical tumors
Ohgaki, H., Kleihues, P., & Heitz, P. U. (1993) · International Journal of Cancer · doi:10.1002/ijc.2910540310 · Cited by 139
Analysis of Wild-Type and Mutant p21 WAF-1 Gene Activities
Lin, J., Reichner, C., Wu, X., & J. Levine, A. (1996) · Molecular and Cellular Biology · doi:10.1128/mcb.16.4.1786 · Cited by 111
Targeting Therapies for the p53 Protein in Cancer Treatments
Levine, A. J. (2019) · Annual Review of Cancer Biology · doi:10.1146/annurev-cancerbio-030518-055455 · Cited by 84
Regulation of Metabolic Activity by p53
Flöter, J., Kaymak, I., & Schulze, A. (2017) · Metabolites · doi:10.3390/metabo7020021 · Cited by 81
McCubrey, J. A., Meher, A. K., Akula, S. M., Abrams, S. L., Steelman, L. S., LaHair, M. M., Franklin, R. A., Martelli, A. M., Ratti, S., Cocco, L., et al. (2022) · Aging · doi:10.18632/aging.204038 · Cited by 12
Metadata
- Authors
- Eliyahu, D., Michalovitz, D., Eliyahu, S., Pinhasi-Kimhi, O., & Oren, M.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1989-11
- Volume
- 86
- Issue
- 22
- Pages
- 8763-8767
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W1991917274
- Cited by
- 692
- References
- 3
- FWCI
- 27.19
- Type
- journal article
- Language
- en
- Open access
- green
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