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Restoration of the tumor suppressor function to mutant p53 by a low-molecular-weight compound
Abstract
The tumor suppressor p53 inhibits tumor growth primarily through its ability to induce apoptosis. Mutations in p53 occur in at least 50% of human tumors. We hypothesized that reactivation of mutant p53 in such tumors should trigger massive apoptosis and eliminate the tumor cells. To test this, we screened a library of low-molecular-weight compounds in order to identify compounds that can restore wild-type function to mutant p53. We found one compound capable of inducing apoptosis in human tumor cells through restoration of the transcriptional transactivation function to mutant p53. This molecule, named PRIMA-1, restored sequence-specific DNA binding and the active conformation to mutant p53 proteins in vitro and in living cells. PRIMA-1 rescued both DNA contact and structural p53 mutants. In vivo studies in mice revealed an antitumor effect with no apparent toxicity. This molecule may serve as a lead compound for the development of anticancer drugs targeting mutant p53.
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In the citing paper
“The small molecule APR-246 (PRIMA-1Met) can reactive mutant p53 in tumor cells and trigger cell death by apoptosis.”
From Inhibition of the glutaredoxin and thioredoxin systems and ribonucleotide reductase by mutant p53-targeting compound APR-246 (2018) · cites this paper as [6]
In the citing paper
“Given that previous studies reported that eprenetapopt induces apoptosis (5, 24), we tested the effect of eprenetapopt in a cell line model incapable of undergoing apoptosis to rule out the dependency on apoptotic machinery for eprenetapopt-induced cell death.”
From Eprenetapopt triggers ferroptosis, inhibits NFS1 cysteine desulfurase, and synergizes with serine and glycine dietary restriction (2022) · cites this paper as [24]
In the citing paper
“our findings are contrary to reports concluding that eprenetapopt induces apoptosis through mut-p53 reactivation (5, 24) and instead supports eprenetapopt as a ferroptosis inducer (20).”
From Eprenetapopt triggers ferroptosis, inhibits NFS1 cysteine desulfurase, and synergizes with serine and glycine dietary restriction (2022) · cites this paper as [24]
In the citing paper
“Importantly, PRIMA-1 and its structural analog PRIMA-1MET (APR-246) inhibited tumor growth in mouse models of GBM [124,129,130].”
From The p53 Pathway in Glioblastoma (2018) · cites this paper as [124]
In the citing paper
“As shown in Figure 5A, RITA and PRIMA-1 increased the expression of the p53 targets p21 and PUMA, based on qPCR measurements at 24 after their addition to cell cultures, similar to previous reports for other p53 mutants [36, 37].”
From Ligand dependent restoration of human TLR3 signaling and death in p53 mutant cells (2016) · cites this paper as [37]
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Metadata
- Authors
- Bykov, V. J. N., Issaeva, N., Shilov, A., Hultcrantz, M., Pugacheva, E., Chumakov, P., Bergman, J., Wiman, K. G., & Selivanova, G.
- Affiliations
- Karolinska University Hospital (SE)
- Engelhardt Institute of Molecular Biology (RU)
- Karolinska Institutet (SE)
- Corresponding author
- Wiman, Klas G.
- ORCID
- Venue
- Nature Medicine
- Published
- 2002-03
- Volume
- 8
- Issue
- 3
- Pages
- 282-288
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W2092902276
- Cited by
- 1,067
- References
- 32
- Citations by year
- 2026: 22 · 2025: 29 · 2024: 42 · 2023: 51 · 2022: 49 · 2021: 58 · 2020: 55 · 2019: 53 · 2018: 51 · 2017: 34 · 2016: 53 · 2015: 42 · 2014: 51 · 2013: 38 · 2012: 37
- FWCI
- 18.33
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- 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
- mutant p53, PRIMA-1, p53 reactivation, tumor suppressor function, apoptosis, transcriptional activation, small molecules, anticancer drug development, DNA binding, p53 conformation, anticancer activity
- MeSH terms
- Animals, Antineoplastic Agents, Aza Compounds, Cell Separation, Flow Cytometry, Humans, Molecular Weight, Mutation, Neoplasms, Organic Chemicals, Protein Conformation, Transplantation, Heterologous, Tumor Cells, Cultured, Molecular Structure, Transcriptional Activation, Tumor Suppressor Protein p53, Apoptosis, Genes, Reporter, Bridged Bicyclo Compounds, Heterocyclic, In Situ Nick-End Labeling, Mice
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