ArticleScientific reports2022
Identification of ubiquitin-specific protease 32 as an oncogene in glioblastoma and the underlying mechanisms.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Deubiquitination of Vangl by USP6 and USP32 Regulates Planar Cell Polarity Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Single-cell RNA sequence analysis reveals USP32 as a therapeutic target to mitigate PD-L1-driven colorectal tumorigenesisTheranostics · 2026Article
- USP32 promotes temporomandibular joint osteoarthritis by modulating PKM2 stability and glycolytic metabolism in chondrocytes.Cell death & disease · 2025Article
- Astragaloside IV regulates FOXM1 deubiquitination to ameliorate trophoblast damage caused by high glucose.Hereditas · 2025Article
- USP32 Promotes Colorectal Carcinoma Progression Through Activating NF-κB Signalling Pathway.Journal of cellular and molecular medicine · 2025Article
- Article
- USP32 facilitates non-small cell lung cancer progression via deubiquitinating BAG3 and activating RAF-MEK-ERK signaling pathway.Oncogenesis · 2024Article
- High USP32 expression contributes to cancer progression and is correlated with immune infiltrates in hepatocellular carcinoma.BMC cancer · 2023Article
- USP32 deubiquitinase: cellular functions, regulatory mechanisms, and potential as a cancer therapy target.Cell death discovery · 2023Review
- Platelet-derived circRNAs signature in patients with gastroenteropancreatic neuroendocrine tumors.Journal of translational medicine · 2023Article
- EGFR endocytosis: more than meets the eye.Oncotarget · 2023Article
- Understanding The Regulatory Role of USP32 and SHMT2 in The Progression of Gastric Cancer.Cell journal · 2023Article
- Review
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
Glioblastoma (GBM) patients present poor prognosis. Deubiquitination by deubiquitinating enzymes (DUBs) is a critical process in cancer progression. Ubiquitin-specific proteases (USPs) constitute the largest sub-family of DUBs. Evaluate the role of USP32 in GBM progression and provide a potential target for GBM treatment. Clinical significance of USP32 was investigated using Gene Expression Omnibus databases. Effects of USP32 on cell growth and metastasis were studied in vitro and in vivo. Differentially expressive genes between USP32-knockdown U-87 MG cells and negative control cells were detected using RNA sequencing and used for Gene Ontology and Kyoto Encyclopedia of Genes and Genomic pathway enrichment analyses. Finally, RT-qPCR was used to validate the divergent expression of genes involved in the enriched pathways. USP32 was upregulated in GBM patients, being correlated to poor prognosis. USP32 downregulation inhibited cell growth and metastasis in vitro. Furthermore, USP32 knockdown inhibited tumorigenesis in vivo. In addition, UPS32 was identified as a crucial regulator in different pathways including cell cycle, cellular senescence, DNA replication, base excision repair, and mismatch repair pathways. USP32 acts as an oncogene in GBM through regulating several biological processes/pathways. It could be a potential target for GBM treatment.
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