ArticleNature communications2024
Mdm2 requires Sprouty4 to regulate focal adhesion formation and metastasis independent of p53.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Topotecan Synergizes with SP141 in the Management of Uveal Melanoma.bioRxiv : the preprint server for biology · 2026Article
- Oncogenic driver and therapeutic target: Prolactin signalling axis in retroperitoneal sarcoma.Clinical and translational medicine · 2026Article
- MDM4 at the Crossroads: Beyond p53 and MDM2.Cancers · 2026Review
- Use of Biomimetic Hydrogels and 3D Cancer Models for Biochemical and Cell Biological Assays.Methods in molecular biology (Clifton, N.J.) · 2026Article
- The multifaceted role of E3 ubiquitin ligases in cancer metastasis: mechanisms, targets, and therapeutic implications.Essays in biochemistry · 2025Review
- MDM2-P53-V-ATPases axis driven by dehydroevodiamine to fight intracellular bacterial infection.Communications biology · 2025Article
- Semaphorin 5A modulates focal adhesion pathway and lamellipodia formation in melanoma.Cell communication and signaling : CCS · 2025Article
- Dual-targeted N-PMIMaterials today. Bio · 2025Article
- The Lysine at Position 177 Is Essential to Limit the Inhibitory Capacities of Sprouty4 Protein in Normal and Cancer-Derived Cells.International journal of molecular sciences · 2025Article
- 3'UTR RNA editing driven by ADAR1 modulates MDM2 expression in breast cancer cells.Functional & integrative genomics · 2025Article
- Protein covariation networks for elucidating ferroptosis inducer mechanisms and potential synergistic drug targets.Communications biology · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
Although the E3 ligase Mdm2 and its homologue and binding partner MdmX are the major regulators of the p53 tumor suppressor protein, it is now evident that Mdm2 and MdmX have multiple functions that do not involve p53. As one example, it is known that Mdm2 can regulate cell migration, although mechanistic insight into this function is still lacking. Here we show in cells lacking p53 expression that knockdown of Mdm2 or MdmX, as well as pharmacological inhibition of the Mdm2/MdmX complex, not only reduces cell migration and invasion, but also impairs cell spreading and focal adhesion formation. In addition, Mdm2 knockdown decreases metastasis in vivo. Interestingly, Mdm2 downregulates the expression of Sprouty4, which is required for the Mdm2 mediated effects on cell migration, focal adhesion formation and metastasis. Further, our findings indicate that Mdm2 dampening of Sprouty4 is a prerequisite for maintaining RhoA levels in the cancer cells that we have studied. Taken together we describe a molecular mechanism whereby the Mdm2/MdmX complex through Sprouty4 regulates cellular processes leading to increase metastatic capability independently of p53.
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