MDM4 is a key therapeutic target in cutaneous melanoma
Open accessAbstract
The inactivation of the p53 tumor suppressor pathway, which often occurs through mutations in TP53 (encoding tumor protein 53) is a common step in human cancer. However, in melanoma-a highly chemotherapy-resistant disease-TP53 mutations are rare, raising the possibility that this cancer uses alternative ways to overcome p53-mediated tumor suppression. Here we show that Mdm4 p53 binding protein homolog (MDM4), a negative regulator of p53, is upregulated in a substantial proportion (∼65%) of stage I-IV human melanomas and that melanocyte-specific Mdm4 overexpression enhanced tumorigenesis in a mouse model of melanoma induced by the oncogene Nras. MDM4 promotes the survival of human metastatic melanoma by antagonizing p53 proapoptotic function. Notably, inhibition of the MDM4-p53 interaction restored p53 function in melanoma cells, resulting in increased sensitivity to cytotoxic chemotherapy and to inhibitors of the BRAF (V600E) oncogene. Our results identify MDM4 as a key determinant of impaired p53 function in human melanoma and designate MDM4 as a promising target for antimelanoma combination therapy.
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Elevated MDMX mRNA is detected in 65% of retinoblastomas, and the same percentage of cutaneous melanomas overexpress MDMX protein.
“Elevated levels of levels of MDMX mRNA are detected in 65% of retinoblastomas and the same percentage of cutaneous melanomas overexpress MDMX protein.21,22”
From Mdmx promotes genomic instability independent of p53 and Mdm2 (2015) · cites this paper as [21]
Elevated Mdmx levels are observed in many tumors and during tumorigenesis.
“elevated Mdmx levels are observed in many tumors.3,18–22”
From Mdmx promotes genomic instability independent of p53 and Mdm2 (2015) · cites this paper as [21]
Melanoma rarely has TP53 mutations, but about 65% of melanomas have high MDM4 levels.
“Melanoma is another tumor in which TP53 is rarely mutated, but approximately 65% of these tumors also have high levels of MDM4 (Gembarska, et al., 2012).”
From The Mdm network and its regulation of p53 activities: a rheostat of cancer risk (2014) · cites this paper as Gembarska, et al., 2012
MDM4 is overexpressed in many human cancers.
“As with MDM2, MDM4 is overexpressed in many human cancers (Danovi, et al., 2004; Gembarska, et al., 2012; Han, et al., 2007; Leventaki, et al., 2012; Ramos, et al., 2001; Riemenschneider, et al., 1999; Valentin-Vega, et al., 2007; Wade, et al., 2013).”
From The Mdm network and its regulation of p53 activities: a rheostat of cancer risk (2014) · cites this paper as Gembarska, et al., 2012
MDM2 and MDMX are deregulated in many human cancers and act oncogenically mainly by inhibiting p53.
“The MDM2 and MDMX (also known as HDMX and MDM4) proteins are deregulated in many human cancers and exert their oncogenic activity predominantly by inhibiting the p53 tumour suppressor.”
From MDM2, MDMX and p53 in oncogenesis and cancer therapy (2013) · cites this paper as [10]
Amplification of MDM genes or altered expression of MDM proteins is a feature of many tumours.
“Amplification of MDM genes or altered expression of MDM proteins is a feature of many tumours3–10 (Table 1).”
From MDM2, MDMX and p53 in oncogenesis and cancer therapy (2013) · cites this paper as [10]
Many tumours exhibit high MDM2 and MDMX protein levels without increased copy number, including melanoma, Ewing's sarcoma, colon carcinoma and retinoblastoma.
“However, many tumours exhibit high MDM2 and MDMX protein levels without increased copy number. These include melanoma10, Ewing's sarcoma22, colon carcinoma9 and retinoblastoma12,23.”
From MDM2, MDMX and p53 in oncogenesis and cancer therapy (2013) · cites this paper as [10]
Following melanocyte-specific expression of MDMX and RAS, the time to onset of melanomas was reduced and the tumours that developed were more aggressive.
“Following melanocyte-specific expression of MDMX and RAS, the time to onset of melanomas was reduced and the tumours that developed were more aggressive10.”
From MDM2, MDMX and p53 in oncogenesis and cancer therapy (2013) · cites this paper as [10]
SAH-p53-8 is effective at high concentrations in a mouse model of melanoma in which MDMX is overexpressed, increasing cytotoxicity and sensitizing melanomas to cisplatin and vemurafenib.
“Despite these issues, it is noteworthy that SAH-p53-8 is effective at high concentrations in a mouse model of melanoma in which MDMX is overexpressed10. In this model, SAH-p53-8 treatment increased cytotoxicity and sensitized melanomas to the chemotherapeutic agent cisplatin and the BRAF-V600E inhibitor vemurafenib (also known as PLX4032).”
From MDM2, MDMX and p53 in oncogenesis and cancer therapy (2013) · cites this paper as [10]
In melanoma, combining the p53-activating peptide SAH-p53-8 with the BRAF inhibitor PLX4032 increased cytotoxicity more than either agent alone.
“co-treatment of melanomas with the p53-activating stapled peptide SAH-p53-8 and the BRAF inhibitor PLX4032 significantly enhanced cytotoxicity when compared with single-agent treatment10.”
From MDM2, MDMX and p53 in oncogenesis and cancer therapy (2013) · cites this paper as [10]
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- Authors
- Gembarska, A., Luciani, F., Fedele, C., Russell, E. A., Dewaele, M., Villar, S., Zwolinska, A., Haupt, S., de Lange, J., Yip, D., Goydos, J., Haigh, J. J., Haupt, Y., Larue, L., Jochemsen, A., Shi, H., Moriceau, G., Lo, R. S., Ghanem, G., Shackleton, M., Bernal, F., & Marine, J.-C.
- Affiliations
- Vlaams Instituut voor Biotechnologie (BE)
- The University of Melbourne (AU)
- National Institutes of Health (US)
- Centre international de recherche sur le cancer (FR)
- Rutgers Cancer Institute (US)
- Ghent University (BE)
- Centre National de la Recherche Scientifique (FR)
- Leiden University Medical Center (NL)
- University of California, Los Angeles (US)
- Institut Jules Bordet (BE)
- Corresponding author
- Marine, Jean-Christophe
- ORCID
- Venue
- Nature Medicine
- Published
- 2012-07-22
- Volume
- 18
- Issue
- 8
- Pages
- 1239-1247
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC3744207
- OpenAlex
- W2046585589
- Cited by
- 327
- References
- 53
- Citations by year
- 2026: 11 · 2025: 14 · 2024: 16 · 2023: 10 · 2022: 20 · 2021: 18 · 2020: 24 · 2019: 30 · 2018: 14 · 2017: 29 · 2016: 31 · 2015: 36 · 2014: 36 · 2013: 30 · 2012: 8
- FWCI
- 17.41
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Leiden Repository (Leiden University) (submittedVersion)
- Ghent University Academic Bibliography (Ghent University) (submittedVersion)
- Dépôt institutionnel de l'Université libre de Bruxelles (Université Libre de Bruxelles) (submittedVersion)
- Minerva Access (University of Melbourne) (submittedVersion)
- Lirias (submittedVersion)
- Pure Amsterdam UMC (submittedVersion)
- Funders
- Pfizer
- Veski
- Pfizer Australia
- Fonds Wetenschappelijk Onderzoek
- Vlaamse regering
- Fondation contre le Cancer
- National Institutes of Health
- Stand Up To Cancer
- Medical Research Council
- National Health and Medical Research Council (628426, 1026990)
- National Cancer Institute (ZIABC011261)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
- Health Sciences › Medicine › Oncology › Cutaneous Melanoma Detection and Management
- Keywords
- MDM4, cutaneous melanoma, p53 inactivation, p53 pathway, BRAF V600E inhibitors, chemoresistance, metastatic melanoma, tumor suppressor pathways, therapeutic target, combination therapy
- MeSH terms
- Animals, Antineoplastic Agents, Female, Humans, Male, Melanocytes, Melanoma, Melanoma, Experimental, Membrane Proteins, Mice, Inbred C57BL, Mice, Nude, Mice, Transgenic, Neoplasm Proteins, Nuclear Proteins, Proto-Oncogene Proteins, Recombinant Fusion Proteins, Skin Neoplasms, Tumor Stem Cell Assay, Signal Transduction, Keratinocytes, Up-Regulation, Gene Expression Regulation, Neoplastic, Tumor Suppressor Protein p53, Apoptosis, Cell Cycle Proteins, Drug Resistance, Neoplasm, GTP Phosphohydrolases, Xenograft Model Antitumor Assays, Cell Line, Tumor, Proto-Oncogene Proteins B-raf, Mice, Proto-Oncogene Proteins c-mdm2, Cell-Penetrating Peptides
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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