Cited by 765Cancer-related Molecular PathwaysHeat shock proteins researchPI3K/AKT/mTOR signaling in cancer

Inhibiting the p53–MDM2 interaction: an important target for cancer therapy

Chène, Patrick·2003·Nature Reviews Cancer

Abstract

p53 is an attractive therapeutic target in oncology because its tumour-suppressor activity can be stimulated to eradicate tumour cells. Inhibiting the p53-MDM2 interaction is a promising approach for activating p53, because this association is well characterized at the structural and biological levels. MDM2 inhibits p53 transcriptional activity, favours its nuclear export and stimulates its degradation, so inhibiting the p53-MDM2 interaction with synthetic molecules should lead to p53-mediated cell-cycle arrest or apoptosis in p53-positive stressed cells.

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Crossref · 10.1038/nrc991

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  • MDM2 binds to the N-terminus of the transcriptional activation domain of p53, inhibiting the trans-activation of p53 and cell growth, regulating cell cycle and inducing cell apoptosis.

    “MDM2 binds to the N-terminus of the transcriptional activation domain of p53, inhibiting the trans-activation of p53 and cell growth, regulating cell cycle and inducing cell apoptosis.365–368”

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Authors
Chène, P.
Venue
Nature Reviews Cancer
Published
2003-02
Volume
3
Issue
2
Pages
102-109
ISSN
  • 1474-175X (ISSN-L)
  • 1474-1768
OpenAlex
W2023486531
Cited by
765
References
78
Citations by year
2026: 17 · 2025: 42 · 2024: 37 · 2023: 46 · 2022: 42 · 2021: 35 · 2020: 27 · 2019: 33 · 2018: 30 · 2017: 31 · 2016: 31 · 2015: 28 · 2014: 45 · 2013: 31 · 2012: 34
FWCI
4.55
Type
journal article
Language
en
Open access
closed
Locations
  • Nature reviews. Cancer (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
Keywords
p53, MDM2, p53-MDM2 interaction, p53 activation, cancer therapy, tumour suppressor, cell cycle arrest, apoptosis, p53 degradation, nuclear export, small molecule inhibitors
MeSH terms
Antineoplastic Agents, Cell Cycle, Humans, Neoplasm Proteins, Neoplasms, Nuclear Proteins, Proto-Oncogene Proteins, Genes, p53, Tumor Suppressor Protein p53, Apoptosis, Active Transport, Cell Nucleus, Proto-Oncogene Proteins c-mdm2

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