ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
SUMOylation of SETD8 Promotes Tumor Growth by Methylating and Stabilizing MYC in Bladder Cancer.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- KMT5a-Mediated IRF3 Stabilization Enhances Macrophage Chemotaxis and Renal Fibrosis Progression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Protein modification systems as cancer biomarkers and therapeutic targets.Precision clinical medicine · 2026Review
- Identification of MYC co-expression gene: POLR3G is associated with cell senescence, immunotherapy, chemotherapy responses, and clinical prognosis in bladder cancer patients.Translational oncology · 2026Article
- ATAD3A promotes bladder cancer progression by regulating glycolysis through MYC stabilization.Journal of translational medicine · 2026Article
- Chromatin Remodeling, DNA Double-Strand Break Repair, and Human Disease: How a Breakup Changes You.Biomolecules · 2026Review
- The lysine methyltransferase KMT5a and p53 regulate the expression of the key autophagy adaptor p62/SQSTM1 in glioblastoma.Cell communication and signaling : CCS · 2026Article
- Transcriptional activation of ALOX5 by c-Myc drives malignant progression and M2 macrophage polarization in clear cell renal cell carcinoma.American journal of cancer research · 2026Article
- HDAC2 as a therapeutic target in bladder cancer: insights into the altered epigenetic regulation and lysine lactylation.Journal of experimental & clinical cancer research : CR · 2025Article
- Non-Histone Lysine Modifications in Tumor Microenvironment: Mechanisms and Therapeutic Opportunities.International journal of molecular sciences · 2025Review
- Multiple functions of the lysine methyltransferase KMT5a in cancer: potential targets for innovative therapies.Clinical epigenetics · 2025Review
- SUMOylation of SETD8 Promotes Tumor Growth by Methylating and Stabilizing MYC in Bladder Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Histone Methyltransferase SETD1B Maintains Cancer Stem Cell Niche by Regulating the Crosstalk between CD24 and Surface Adhesion Molecules in Hepatocellular Carcinoma.International journal of biological sciences · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Aberrant transcriptional and epigenetic landscape plays crucial roles in the progression of bladder cancer (BC). However, effective therapeutic targets derived from these processes remain undeveloped. This study pinpoints SET-domain-containing protein 8 (SETD8) as a pivotal gene that promotes bladder tumor growth through a screening with a CRISPR-Cas9 library targeting transcriptional and epigenetic factors. BC patient samples display elevated SETD8 protein expression, and higher expression of SETD8 correlates with poorer prognosis. Further, MYC is identified as a novel substrate for SETD8. Specifically, SETD8 methylates MYC at lysine 412 (K412), disrupting the interaction between MYC and the E3 ubiquitin ligase CHIP, which results in MYC stabilization and ultimately promotes tumor growth both in vitro and in vivo. Moreover, this study uncovers that SUMOylation of SETD8 leads to SETD8 stabilization. The SUMOylated SETD8 further enhances MYC methylation and stabilization via SUMO-SIM interaction. Knocking down SETD8 or using the SETD8 specific inhibitor UNC0379 substantially reduces the protein level of MYC and inhibits the bladder tumor growth in vitro and in vivo. These findings provide strong support for the idea that targeting the SETD8/MYC axis offers a promising therapeutic approach for BC patient.
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