The Mdm2–p53 relationship evolves: Mdm2 swings both ways as an oncogene and a tumor suppressor
Open accessAbstract
Mdm2 has been well characterized as a negative regulator of the tumor suppressor p53. Recent studies have shown that Mdm2 is activated in response to a variety of oncogenic pathways independent of p53. Although its role as an oncogene via suppression of p53 function remains clear, growing evidence argues for p53-independent effects, as well as the remarkable possibility that Mdm2 has tumor suppressor functions in the appropriate context. Hence, Mdm2 is proving to be a key player in human cancer in its own right, and thus an important target for therapeutic intervention.
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As an E3 ubiquitin ligase, Mdm2 mediates ubiquitination and 26S proteasomal degradation of p53.
“Furthermore, as E3 ubiquitin ligase, Mdm2 leads to the ubiquitination and degradation of p53 by the 26S proteasome. 1”
From Mdm2 inhibitors synergize with topoisomerase II inhibitors to induce p53-independent pancreatic cancer cell death (2013) · cites this paper as [1]
Binding of Mdm2 to the N-terminus of p53 inhibits the transactivation domain of p53.
“Binding of Mdm2 to the N-terminus of p53 inhibits the transactivation domain of the tumor suppressor.”
From Mdm2 inhibitors synergize with topoisomerase II inhibitors to induce p53-independent pancreatic cancer cell death (2013) · cites this paper as [1]
Mdm2 acts as a critical negative regulator of the tumor suppressor p53.
“Murine double minute 2 [Mdm2; termed as human double minute 2 (HDM2) in Homo sapiens] is a critical negative regulator of the transcription factor and tumor suppressor p53. 1”
From Mdm2 inhibitors synergize with topoisomerase II inhibitors to induce p53-independent pancreatic cancer cell death (2013) · cites this paper as [1]
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References 107 · Cited by 344
- Authors
- Manfredi, J. J.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- Corresponding author
- Manfredi, James J.
- ORCID
- Manfredi, James J.
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2010-08-01
- Volume
- 24
- Issue
- 15
- Pages
- 1580-1589
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- PMC
- PMC2912554
- OpenAlex
- W2103237568
- Cited by
- 344
- References
- 107
- Citations by year
- 2026: 9 · 2025: 14 · 2024: 7 · 2023: 9 · 2022: 14 · 2021: 25 · 2020: 19 · 2019: 17 · 2018: 22 · 2017: 20 · 2016: 26 · 2015: 31 · 2014: 35 · 2013: 27 · 2012: 51
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (R01CA086001, R01CA125741, P01CA080058)
- 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
- MDM2, p53, tumor suppressor, oncogenes, cancer therapy targets
- MeSH terms
- Animals, Cell Differentiation, Epithelial Cells, Humans, Oncogenes, Gene Expression Regulation, Neoplastic, Genes, Tumor Suppressor, Tumor Suppressor Protein p53, Apoptosis, Cell Proliferation, Proto-Oncogene Proteins c-mdm2
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