ArticleNature communications2024
Stabilization of Pin1 by USP34 promotes Ubc9 isomerization and protein sumoylation in glioma stem cells.
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 27 papers.
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Who cites it
27 citing papers in PubMed, 39 citations in OpenAlex.
- The Effect of Prolyl Isomerase Pin1 on the Development of Metabolic Dysfunction-Associated Steatohepatitis and a New Treatment Strategy.International journal of molecular sciences · 2026Review
- Sevoflurane ameliorates cerebral ischemia-reperfusion injury by modulating mitochondrial dynamics and attenuating apoptosis via Shh-YAP1 signaling pathway.Molecular brain · 2026Article
- Targeting SUMOylation in glioblastoma: A novel avenue for therapy and biomarker discovery.Genes & diseases · 2026Review
- UBC9-mediated p53 SUMOylation drives tubular senescence and exacerbates acute kidney injury in mice.Acta pharmacologica Sinica · 2026Article
- UBC9-mediated SUMOylation of CORO1C drives lung adenocarcinoma progression via Arp2/3-dependent cytoskeletal remodeling.Cell death & disease · 2026Article
- SAE1 emerges as a pan-cancer driver and key regulator of HCC metastasis.Journal of advanced research · 2026Article
- USP34 attenuates cartilage degradation in temporomandibular joint osteoarthritis by ANT1-mediated mitophagy.JBMR plus · 2026Article
- Dysregulation of post-translational modifications in glioma: advances in pathological mechanisms and clinical targeting strategies.Journal of translational medicine · 2026Review
- EGFR/ZBED1 reciprocal regulation promotes stemness and tumorigenesis in glioblastoma.Neuro-oncology · 2026Article
- Dual Regulation of Post-Translational Modification of Proteins: Bottlenecks and Breakthroughs in NK Cell Therapy for Glioblastoma.International journal of general medicine · 2026Review
- Inhibition of CDK1 Promotes Immunogenic Cell Death in Neuroblastoma.Cancer management and research · 2026Article
- DAZAP1 promotes cancer progression and chemotherapy resistance by stabilizing PIN1 protein in gastric cancer.Cell biology and toxicology · 2025Article
- Immunoregulatory Roles of Tumor-Originated Pericytes Identified by Single-Cell Analysis in Glioblastoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Neurodegeneration rewires the tumor microenvironment via the neuro-immune-cancer axis.iScience · 2025Review
- UBC9 overexpression promotes proliferation and metastasis in gastric cancer via ATF2.World journal of surgical oncology · 2025Article
- USP39 promote post-translational modifiers to stimulate the progress of cancer.Discover oncology · 2025Review
- UBC9: a novel therapeutic target in papillary thyroid carcinoma.Journal of endocrinological investigation · 2025Article
- Histone Lactylation-Driven Ubiquitin-Specific Protease 34 Promotes Cisplatin Resistance in Hepatocellular Carcinoma.Gastroenterology research · 2025Article
- Lactylation-related gene signatures identify glioma molecular subtypes with prognostic, immunological, and therapeutic implications.Frontiers in oncology · 2025Article
- Roles of deubiquitinases in urologic cancers (Review).Oncology letters · 2024Review
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 1 country.
Funding
Abstract
The peptidyl-prolyl cis-trans isomerase Pin1 is a pivotal therapeutic target in cancers, but the regulation of Pin1 protein stability is largely unknown. High Pin1 expression is associated with SUMO1-modified protein hypersumoylation in glioma stem cells (GSCs), but the underlying mechanisms remain elusive. Here we demonstrate that Pin1 is deubiquitinated and stabilized by USP34, which promotes isomerization of the sole SUMO E2 enzyme Ubc9, leading to SUMO1-modified hypersumoylation to support GSC maintenance. Pin1 interacts with USP34, a deubiquitinase with preferential expression and oncogenic function in GSCs. Such interaction is facilitated by Plk1-mediated phosphorylation of Pin1. Disruption of USP34 or inhibition of Plk1 promotes poly-ubiquitination and degradation of Pin1. Furthermore, Pin1 isomerizes Ubc9 to upregulate Ubc9 thioester formation with SUMO1, which requires CDK1-mediated phosphorylation of Ubc9. Combined inhibition of Pin1 and CDK1 with sulfopin and RO3306 most effectively suppresses orthotopic tumor growth. Our findings provide multiple molecular targets to induce Pin1 degradation and suppress hypersumoylation for cancer treatment.
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