Cited by 1,987Cancer-related Molecular PathwaysCell death mechanisms and regulationPI3K/AKT/mTOR signaling in cancer

The p53 proto-oncogene can act as a suppressor of transformation

Finlay, Cathy A., Hinds, Philip W., Levine, Arnold J.·1989·Cell

Abstract

DNA clones of the wild-type p53 proto-oncogene inhibit the ability of E1A plus ras or mutant p53 plus ras-activated oncogenes to transform primary rat embryo fibroblasts. The rare clones of transformed foci that result from E1A plus ras plus wild-type p53 triple transfections all contain the p53 DNA in their genome, but the great majority fail to express the p53 protein. The three cell lines derived from such foci that express p53 all produce mutant p53 proteins with properties similar or identical to transformation-activated p53 proteins. The p53 mutants selected in this fashion (transformation in vitro) resemble the p53 mutants selected in tumors (in vivo). These results suggest that the p53 proto-oncogene can act negatively to block transformation.

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Crossref · 10.1016/0092-8674(89)90045-7

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  • Mut-p53 can exert a dominant-negative regulation over wild type p53 through protein-protein interactions and the formation of oligomeric complexes.

    “Further sustaining its tumorigenic effect, mut-p53 can exert a dominant-negative regulation over wt-p53 through protein-protein interactions and the formation of oligomeric complexes [78,79].”

    From The p53 Pathway in Glioblastoma (2018) · cites this paper as [79]

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Authors
Finlay, C. A., Hinds, P. W., & Levine, A. J.
Affiliations
Princeton University (US)
Venue
Cell
Publisher
Elsevier BV
Published
1989-06
Volume
57
Issue
7
Pages
1083-1093
ISSN
0092-8674 (ISSN-L)
OpenAlex
W2163565167
Cited by
1,987
References
70
Citations by year
2026: 14 · 2025: 12 · 2024: 25 · 2023: 27 · 2022: 20 · 2021: 34 · 2020: 37 · 2019: 31 · 2018: 29 · 2017: 29 · 2016: 28 · 2015: 12 · 2014: 28 · 2013: 26 · 2012: 38
FWCI
79.38
Type
journal article
Language
en
Open access
closed
Locations
  • Cell (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Cancer Institute (P01CA041086, P01-CA41086-03)
Topics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
Keywords
tumor suppressor, oncogenic transformation, adenovirus E1A, oncogenic Ras, mutant p53, p53 expression, rat embryo fibroblasts, transformed foci, tumor suppressor function
MeSH terms
Animals, Antigens, Polyomavirus Transforming, Cell Line, Cell Transformation, Neoplastic, Cells, Cultured, Gene Expression Regulation, Neoplasm Proteins, Oncogene Proteins, Viral, Phosphoproteins, Proto-Oncogene Proteins, Genes, ras, Transfection, Tumor Suppressor Protein p53, Adenovirus Early Proteins, Mice, Rats

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