Cited by 146Cancer-related Molecular PathwaysCell death mechanisms and regulationHeat shock proteins research

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Cancer-derived p53 mutants suppress p53-target gene expression--potential mechanism for gain of function of mutant p53

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Vikhanskaya, F., Lee, M. K., Mazzoletti, M., Broggini, M., Sabapathy, K.·2007·Nucleic Acids Research

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Abstract

Tumour-derived p53 mutants are thought to have acquired 'gain-of-function' properties that contribute to oncogenicity. We have tested the hypothesis that p53 mutants suppress p53-target gene expression, leading to enhanced cellular growth. Silencing of mutant p53 expression in several human cell lines was found to lead to the upregulation of wild-type p53-target genes such as p21, gadd45, PERP and PTEN. The expression of these genes was also suppressed in H1299-based isogenic cell lines expressing various hot-spot p53 mutants, and silencing of mutant p53, but not TAp73, abrogated the suppression. Consistently, these hot-spot p53 mutants were able to suppress a variety of p53-target gene promoters. Analysis using the proto-type p21 promoter construct indicated that the p53-binding sites are dispensable for mutant p53-mediated suppression. However, treatment with the histone deacetylase inhibitor trichostatin-A resulted in relief of mutant p53-mediated suppression, suggesting that mutant p53 may induce hypo-acetylation of target gene promoters leading to the suppressive effects. Finally, we show that stable down-regulation of mutant p53 expression resulted in reduced cellular colony growth in human cancer cells, which was found to be due to the induction of apoptosis. Together, the results demonstrate another mechanism through which p53 mutants could promote cellular growth.

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Surfing the p53 network
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“Mutated p53 is often overexpressed in tumour cells (1,2,6), due to their inability to effectively activate MDM2, which negatively regulates p53 abundance (7,8).”
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Authors: Vikhanskaya, F., Lee, M. K., Mazzoletti, M., Broggini, M., & Sabapathy, K.
Affiliations: National Cancer Centre Singapore (SG)
National University of Singapore (SG)
Corresponding author: Sabapathy, K.
ORCID: Lee, M. K.
Broggini, M.
Sabapathy, K.
Venue: Nucleic Acids Research
Publisher: Oxford University Press (OUP)
Published: 2007-03-01
Volume: 35
Issue: 6
Pages: 2093-2104
ISSN: 0305-1048 (ISSN-L)
1362-4962
DOI: 10.1093/nar/gkm099
PMC: PMC1874625
OpenAlex: W2111523470
Cited by: 145
References: 38
Citations by year: 2026: 3 · 2025: 11 · 2024: 8 · 2023: 6 · 2022: 6 · 2021: 4 · 2020: 8 · 2019: 6 · 2018: 9 · 2017: 9 · 2016: 12 · 2015: 10 · 2014: 12 · 2013: 11 · 2012: 4
FWCI: 3.21
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by-nc
Locations: Nucleic Acids Research (publishedVersion, cc-by-nc)
PubMed Central (publishedVersion, cc-by-nc)
PubMed (publishedVersion)
National University of Singapore (submittedVersion)
Funders: Medical Research Council
National Medical Research Council
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 › Heat shock proteins research
Keywords: mutant p53, gain-of-function, p21, GADD45, PERP, PTEN, p53 binding sites, histone deacetylation, trichostatin A, apoptosis, cell growth, TAp73
MeSH terms: Binding Sites, Enzyme Inhibitors, Humans, Hydroxamic Acids, Mutation, Neoplasms, Promoter Regions, Genetic, Down-Regulation, Gene Expression Regulation, Neoplastic, Genes, p53, Tumor Suppressor Protein p53, Apoptosis, RNA Interference, Cell Line, Tumor, Cyclin-Dependent Kinase Inhibitor p21, Histone Deacetylase Inhibitors

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Cancer-derived p53 mutants suppress p53-target gene expression--potential mechanism for gain of function of mutant p53

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