ArticleCell cycle (Georgetown, Tex.)2015
c-Myc is targeted to the proteasome for degradation in a SUMOylation-dependent manner, regulated by PIAS1, SENP7 and RNF4.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 96 citations in OpenAlex.
- Understanding and Overcoming Osteosarcoma Heterogeneity.Biomolecules · 2026Review
- Crotonylation impedes c-Myc oncogenic activity.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Dynamic sumoylation is essential in yeast for suppressing stress-induced gene expression in non-stress conditions.Nucleic acids research · 2026Article
- Blockage of SUMO E1 enzyme inhibits ocular lens fibrosis by mediating SMAD4 SUMOylation.Genes & diseases · 2026Article
- Proteasomal control of transcription factors: mechanisms, regulation and dysregulation.Cellular and molecular life sciences : CMLS · 2026Review
- SUMOylation is destined for regulatory T cell-related immune dysregulation.Cell death discovery · 2026Review
- Colorectal Cancer Cell's Weapon: RNF32 Engages SPP1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Fatty Acid Synthase as a Potential Metabolic Vulnerability in Ocular Adnexal Sebaceous Carcinoma.Cancers · 2026Article
- Cryo-EM structures reveal the molecular mechanism of SUMO E1-E2 thioester transfer.Nature structural & molecular biology · 2025Article
- NKD1 enhances colon cancer progression by inhibiting the autophagic degradation of MYC.Cell death & disease · 2025Article
- Targeting SUMOylation in ovarian cancer: Sensitivity, resistance, and the role of MYC.iScience · 2025Article
- RNF112 Facilitates Ubiquitin-Mediated Degradation of c-Myc, Suppressing Proliferation, Migration and Lipid Synthesis in Bladder Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Roles of Post-Translational Modifications of Transcription Factors Involved in Breast Cancer Hypoxia.Molecules (Basel, Switzerland) · 2025Review
- Review
- Mouse and human embryonic genome activation initiate at the one-cell stage.Frontiers in cell and developmental biology · 2025Article
- Crosstalk between SUMOylation and other post-translational modifications in breast cancer.Cellular & molecular biology letters · 2024Review
- Substrate and Functional Diversity of Protein Lysine Post-translational Modifications.Genomics, proteomics & bioinformatics · 2024Review
- Genomic Analysis of Lymphoma Risk in Bullmastiff Dogs.Veterinary sciences · 2023Article
- The SUMOylation and ubiquitination crosstalk in cancer.Journal of cancer research and clinical oncology · 2023Review
- MYC acetylated lysine residues drive oncogenic cell transformation and regulate select genetic programs for cell adhesion-independent growth and survival.Genes & development · 2023Article
14 more citing papers are in PubMed but not listed here.
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5 authors at 1 institution in 1 country.
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Abstract
c-Myc is the most frequently overexpressed oncogene in tumors, including breast cancer, colon cancer and lung cancer. Post-translational modifications comprising phosphorylation, acetylation and ubiquitylation regulate the activity of c-Myc. Recently, it was shown that c-Myc-driven tumors are strongly dependent on the SUMO pathway. Currently, the relevant SUMO target proteins in this pathway are unknown. Here we show that c-Myc is a target protein for SUMOylation, and that SUMOylated c-Myc is subsequently ubiquitylated and degraded by the proteasome. SUMO chains appeared to be dispensable for this process, polymerization-deficient SUMO mutants supported proteolysis of SUMOylated c-Myc. These results indicate that multiple SUMO monomers conjugated to c-Myc could be sufficient to direct SUMOylated c-Myc to the ubiquitin-proteasome pathway. Knocking down the SUMO-targeted ubiquitin ligase RNF4 enhanced the levels of SUMOylated c-Myc, indicating that RNF4 could recognize a multi-SUMOylated protein as a substrate in addition to poly-SUMOylated proteins. Knocking down the SUMO E3 ligase PIAS1 resulted in reduced c-Myc SUMOylation and increased c-Myc transcriptional activity, indicating that PIAS1 mediates c-Myc SUMOylation. Increased SUMOylation of c-Myc was noted upon knockdown of the SUMO protease SENP7, indicating that it also could regulate a multi-SUMOylated protein in addition to poly-SUMOylated proteins. C-Myc lacks KxE-type SUMOylation consensus motifs. We used mass spectrometry to identify 10 SUMO acceptor lysines: K52, K148, K157, K317, K323, K326, K389, K392, K398 and K430. Intriguingly, mutating all 10 SUMO acceptor lysines did not reduce c-Myc SUMOylation, suggesting that SUMO acceptor lysines in c-Myc act promiscuously. Our results provide novel insight into the complexity of c-Myc post-translational regulation.
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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.