ArticleOncogene2024
DLGAP5 triggers proliferation and metastasis of bladder cancer by stabilizing E2F1 via USP11.
Article in Oncogene, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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
16 citing papers in PubMed, 21 citations in OpenAlex.
- POC1A promotes the proliferation, metastasis and stemness of bladder cancer by stabilizing BMI1 via USP7.Oncogene · 2026Article
- YY1-induced upregulation of DLGAP5 promotes tumor progression in lung adenocarcinoma via Wnt/β-catenin/EMT pathway.Journal of translational medicine · 2026Article
- The Rac1-USP11 feedback amplification loop: a radiation-activated engine driving radioresistance in hepatocellular carcinoma.British journal of cancer · 2026Article
- A telomere-based prognostic model incorporating E2F1, MYCN, VPS72, CFAP53, OR8A1, and TXNRD1 for hepatocellular carcinoma.European journal of medical research · 2026Article
- DLGAP5 promotes salivary adenoid cystic carcinoma proliferation and metastasis through PI3K/AKT pathway.American journal of cancer research · 2026Article
- Differentially Expressed Genes Associated with the Development of Cervical Cancer.International journal of molecular sciences · 2025Article
- USP43 promotes gemcitabine resistance by regulating cholesterol homeostasis through E2F1 stabilization in bladder cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- Regulation of drug resistance in bladder urothelial carcinoma by tumor aerobic glycolysis.Journal of translational medicine · 2025Review
- Spotlight onGenes · 2025Article
- MELK as a Mediator of Stemness and Metastasis in Aggressive Subtypes of Breast Cancer.International journal of molecular sciences · 2025Article
- Identification of exosome-related genes associated with prognosis and immune infiltration features in pancreatic cancer.Discover oncology · 2025Article
- DLGAP5 Promotes Acute Liver Injury via Hepatocyte Pyroptosis-Driven Macrophage Metabolic Reprogramming and M1 Polarization.International journal of biological sciences · 2025Article
- Identification and validation of shared biomarkers and drug repurposing in psoriasis and Crohn's disease: integrating bioinformatics, machine learning, and experimental approaches.Frontiers in immunology · 2025Article
- DLGAP5 enhances bladder cancer chemoresistance by regulating glycolysis through MYC stabilization.Theranostics · 2025Article
- Deubiquitylase USP52 Promotes Bladder Cancer Progression by Modulating Ferroptosis through Stabilizing SLC7A11/xCT.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Therapeutic target genes and regulatory networks of gallic acid in cervical cancer.Frontiers in genetics · 2024Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bladder cancer (BLCA) is one of the most widespread malignancies worldwide, and displays significant tumor heterogeneity. Understanding the molecular mechanisms exploitable for treating aggressive BLCA represents a crucial objective. Despite the involvement of DLGAP5 in tumors, its precise molecular role in BLCA remains unclear. BLCA tissues exhibit a substantial increase in DLGAP5 expression compared with normal bladder tissues. This heightened DLGAP5 expression positively correlated with the tumor's clinical stage and significantly affected prognosis negatively. Additionally, experiments conducted in vitro and in vivo revealed that alterations in DLGAP5 expression notably influence cell proliferation and migration. Mechanistically, the findings demonstrated that DLGAP5 was a direct binding partner of E2F1 and that DLGAP5 stabilized E2F1 by preventing the ubiquitination of E2F1 through USP11. Furthermore, as a pivotal transcription factor, E2F1 fosters the transcription of DLGAP5, establishing a positive feedback loop between DLGAP5 and E2F1 that accelerates BLCA development. In summary, this study identified DLGAP5 as an oncogene in BLCA. Our research unveils a novel oncogenic mechanism in BLCA and offers a potential target for both diagnosing and treating BLCA.
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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 Socratic graph.