ArticleAmerican journal of cancer research2012
High levels of Hdmx promote cell growth in a subset of uveal melanomas.
Article in American journal of cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Beyond sex determination: the Y chromosome in male cancers.Nature reviews. Cancer · 2026Review
- The role of signaling pathways mediated by the GPCRs CysLTR1/2 in melanocyte proliferation and senescence.Science signaling · 2024Review
- CEP-1347 Dually Targets MDM4 and PKC to Activate p53 and Inhibit the Growth of Uveal Melanoma Cells.Cancers · 2023Article
- Preclinical Evaluation of Trabectedin in Combination With Targeted Inhibitors for Treatment of Metastatic Uveal Melanoma.Investigative ophthalmology & visual science · 2022Article
- MDMX Regulates Transcriptional Activity of p53 and FOXO Proteins to Stimulate Proliferation of Melanoma Cells.Cancers · 2022Article
- The MDM2 Inhibitor Navtemadlin Arrests Mouse Melanoma GrowthCancer research communications · 2022Article
- Targeting MDM4 as a Novel Therapeutic Approach in Prostate Cancer Independent of p53 Status.Cancers · 2022Article
- Functional proteomic analysis reveals roles for PKCδ in regulation of cell survival and cell death: Implications for cancer pathogenesis and therapy.Advances in biological regulation · 2020Article
- The long and the short of it: the MDM4 tail so far.Journal of molecular cell biology · 2019Review
- Article
- The role of MDM2 and MDM4 in breast cancer development and prevention.Journal of molecular cell biology · 2017Review
- MDMX under stress: the MDMX-MDM2 complex as stress signals hub.Translational cancer research · 2016Article
- MDMX (MDM4), a Promising Target for p53 Reactivation Therapy and Beyond.Cold Spring Harbor perspectives in medicine · 2016Review
- Dual inhibition of protein kinase C and p53-MDM2 or PKC and mTORC1 are novel efficient therapeutic approaches for uveal melanoma.Oncotarget · 2016Article
- Identification of a Small Molecule That Overcomes HdmX-Mediated Suppression of p53.Molecular cancer therapeutics · 2016Article
- Antisense oligonucleotide-mediated MDM4 exon 6 skipping impairs tumor growth.The Journal of clinical investigation · 2016Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
The p53 tumor suppressor pathway is inactivated in cancer either via direct mutation or via deregulation of upstream regulators or downstream effectors. P53 mutations are rare in uveal melanoma. Here we investigated the role of the p53 inhibitor Hdmx in uveal melanoma. We found Hdmx over-expression in a subset of uveal melanoma cell lines and fresh-frozen tumor samples. Hdmx depletion resulted in cell-line dependent growth inhibition, apparently correlating with differential Hdm2 levels. Surprisingly, p53 knockdown hardly rescued cell cycle arrest and apoptosis induction upon Hdmx knockdown, whereas it effectively prevented growth suppression induced by the potent p53 activator Nutlin-3. In addition, two compounds inhibiting Hdmx function or expression, SAH-p53-8 and XI-011, also elicited a growth inhibitory effect in a partly p53-independent manner. These findings suggest a novel, growth-promoting function of Hdmx that does not rely on its ability to inhibit p53. We provide evidence for a contribution of p27 protein induction to the observed p53-independent G1 arrest in response to Hdmx knockdown. In conclusion, our study establishes the importance of Hdmx as an oncogene in a subset of uveal melanomas and widens the spectrum of its function beyond p53 inhibition.
Indexed as
Identifiers
22957303PMC3433101W1585215516What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.