ArticleNature communications2020
Tumor derived UBR5 promotes ovarian cancer growth and metastasis through inducing immunosuppressive macrophages.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers, 3 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
114 citing papers in PubMed, 3 syntheses or guidelines pooled it, 165 citations in OpenAlex.
- The Impact of Chronic Stress on Treatment Outcomes of Cancer Patients with Divergent Survival Rates: A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Unraveling the role of M2 TAMs in ovarian cancer dynamics: a systematic review.Journal of translational medicine · 2025Pooled it
- Hyperthermic intraperitoneal chemotherapy enhances survival outcomes in primary ovarian cancer following cytoreductive surgery: a systematic review and meta-analysis.Frontiers in oncology · 2025Pooled it
- E3 Ubiquitin Ligase UBR5 Aggravates Cardiac Hypertrophy Via Inhibiting Nrf2/HO-1 Pathway.Cardiovascular drugs and therapy · 2026Article
- JNK acts as a molecular brake of the CDC73 positive feedback loop to modulate osteosarcoma malignant progression via UBR5.Oncogene · 2026Article
- Pathophysiological roles of monocytes and macrophages in cancer.Nature reviews. Immunology · 2026Review
- Pan-cancer proteogenomic interrogation of the ubiquitin-proteasome system.Cell death and differentiation · 2026Article
- Using biomaterial-based 3D in vitro cancer models to solve current clinical problems.British journal of cancer · 2026Review
- Gemcitabine activates the Hippo signaling pathway and suppresses tumor growth by stabilizing large tumor suppressor kinase 2 through the hypoxia-inducible factor 1-alpha/ubiquitin protein ligase E3 component N-recognin 5 axis.Journal of cell communication and signaling · 2026Article
- SIRT5-dependent desuccinylation licenses UBR5-mediated degradation of TAMM41 to regulate mitochondrial metabolism in lung adenocarcinoma.Biology direct · 2026Article
- Pan-cancer proteogenomic interrogation of the Ubiquitin Proteasome System.bioRxiv : the preprint server for biology · 2026Article
- Ascites circRNA ASCOR Drives Platinum Resistance of High-Grade Serous Ovarian Cancer by Facilitating RPA1 Nuclear Translocation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Identification of RNA processing-related gene-based bladder cancer subtypes for prognosis and immune landscape assessment.Translational andrology and urology · 2026Article
- Identification of novel molecular subtypes in ovarian cancerThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026Article
- UBR5 regulates the progression of colorectal cancer cells through Snail-induced epithelial-mesenchymal transition.Genes & diseases · 2026Article
- Targeting cancer stem cells predicts response and reverses chemoresistance in ascites-derived ovarian cancer organoids.BMC medicine · 2026Article
- Construction of a prognostic model based on protein post-translational modification genes for prediction of immune characteristics and therapeutic response in hepatocellular carcinoma.Discover oncology · 2026Article
- The role of tumor-associated macrophages in cancer development and their significance as prognostic markers.Clinical and experimental medicine · 2026Review
- Proteomic atlas of human peritoneal tissue.Scientific reports · 2026Article
- Hypoxia-driven remodeling of SELENOPNature communications · 2026Article
54 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
Abstract
Immunosuppressive tumor microenvironment (TME) and ascites-derived spheroids in ovarian cancer (OC) facilitate tumor growth and progression, and also pose major obstacles for cancer therapy. The molecular pathways involved in the OC-TME interactions, how the crosstalk impinges on OC aggression and chemoresistance are not well-characterized. Here, we demonstrate that tumor-derived UBR5, an E3 ligase overexpressed in human OC associated with poor prognosis, is essential for OC progression principally by promoting tumor-associated macrophage recruitment and activation via key chemokines and cytokines. UBR5 is also required to sustain cell-intrinsic β-catenin-mediated signaling to promote cellular adhesion/colonization and organoid formation by controlling the p53 protein level. OC-specific targeting of UBR5 strongly augments the survival benefit of conventional chemotherapy and immunotherapies. This work provides mechanistic insights into the novel oncogene-like functions of UBR5 in regulating the OC-TME crosstalk and suggests that UBR5 is a potential therapeutic target in OC treatment for modulating the TME and cancer stemness.
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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.