ArticleGenes & development2017
Gain-of-function mutant p53 activates small GTPase Rac1 through SUMOylation to promote tumor progression.
Article in Genes & development, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 47 citations in OpenAlex.
- Research Progress on the ARHGEF Family in Cardiovascular Diseases.Cell biochemistry and function · 2026Review
- MTSS1-dependent ubiquitin modifications mediated by FBXO44 remodel the actin cytoskeleton to promote gastric cancer progression.Molecular cancer · 2026Article
- The nuclear phosphoinositide-p53 signalosome in the regulation of cell motility.Protein & cell · 2025Review
- Gut microbes and their metabolites in relation to the classic tumor suppressor gene P53: a novel narrative.NPJ biofilms and microbiomes · 2025Review
- p53 in colorectal cancer: from a master player to a privileged therapy target.Journal of translational medicine · 2025Review
- Lipogenic enzyme FASN promotes mutant p53 accumulation and gain-of-function through palmitoylation.Nature communications · 2025Article
- The next decade of SET: from an oncoprotein to beyond.Journal of molecular cell biology · 2024Review
- Cell fate regulation governed by p53: Friends or reversible foes in cancer therapy.Cancer communications (London, England) · 2024Review
- The ubiquitin ligase TRIM21 regulates mutant p53 accumulation and gain of function in cancer.The Journal of clinical investigation · 2023Article
- Leukemia inhibitory factor drives glucose metabolic reprogramming to promote breast tumorigenesis.Cell death & disease · 2022Article
- Hepatic Ischemia-reperfusion Injury in Mice was Alleviated by Rac1 Inhibition - More Than Just ROS-inhibition.Journal of clinical and translational hepatology · 2022Article
- Regulation of p53 Function by Formation of Non-Nuclear Heterologous Protein Complexes.Biomolecules · 2022Review
- Article
- FOXO3a inhibits nephroblastoma cell proliferation, migration and invasion, and induces apoptosis through downregulating the Wnt/β‑catenin signaling pathway.Molecular medicine reports · 2021Article
- The Function of the Mutant p53-R175H in Cancer.Cancers · 2021Review
- Article
- Wrestling and Wrapping: A Perspective on SUMO Proteins in Schwann Cells.Biomolecules · 2021Review
- Tumor suppressor p53 regulates intestinal type 2 immunity.Nature communications · 2021Article
- Plasma Exosome-Derived Sentrin SUMO-Specific Protease 1: A Prognostic Biomarker in Patients With Osteosarcoma.Frontiers in oncology · 2021Article
- LINC00460-miR-149-5p/miR-150-5p-Mutant p53 Feedback Loop Promotes Oxaliplatin Resistance in Colorectal Cancer.Molecular therapy. Nucleic acids · 2020Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Tumor suppressor p53 is frequently mutated in human cancer. Mutant p53 often promotes tumor progression through gain-of-function (GOF) mechanisms. However, the mechanisms underlying mutant p53 GOF are not well understood. In this study, we found that mutant p53 activates small GTPase Rac1 as a critical mechanism for mutant p53 GOF to promote tumor progression. Mechanistically, mutant p53 interacts with Rac1 and inhibits its interaction with SUMO-specific protease 1 (SENP1), which in turn inhibits SENP1-mediated de-SUMOylation of Rac1 to activate Rac1. Targeting Rac1 signaling by RNAi, expression of the dominant-negative Rac1 (Rac1 DN), or the specific Rac1 inhibitor NSC23766 greatly inhibits mutant p53 GOF in promoting tumor growth and metastasis. Furthermore, mutant p53 expression is associated with enhanced Rac1 activity in clinical tumor samples. These results uncover a new mechanism for Rac1 activation in tumors and, most importantly, reveal that activation of Rac1 is an unidentified and critical mechanism for mutant p53 GOF in tumorigenesis, which could be targeted for therapy in tumors containing mutant p53.
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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.