ArticleOncogene2019
RNA splicing factor USP39 promotes glioma progression by inducing TAZ mRNA maturation.
Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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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.
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Who cites it
42 citing papers in PubMed, 64 citations in OpenAlex.
- Splice-switching of the oncogenic BCS1L isoform suppresses ovarian cancer progression by disrupting mitochondrial function.Cell death & disease · 2026Article
- DDX42 Enhances Hepatocellular Carcinoma Cell Proliferation, Radiation and Sorafenib Resistance via Regulating GRB2 RNA Maturation and Activating PI3K/AKT Pathway.Journal of cellular and molecular medicine · 2025Article
- USP39 promote post-translational modifiers to stimulate the progress of cancer.Discover oncology · 2025Review
- Exploring the cancerous nexus: the pivotal and diverse roles of USP39 in cancer development.Discover oncology · 2025Review
- Identification of USP39 as a prognostic and predictive biomarker for determining the response to immunotherapy in pancreatic cancer.BMC cancer · 2025Article
- USP39 phase separates into the nucleolus and drives lung adenocarcinoma progression by promoting GLI1 expression.Cell communication and signaling : CCS · 2025Article
- USP39 at the crossroads of cancer immunity: regulating immune evasion and immunotherapy response through RNA splicing and ubiquitin signaling.Frontiers in immunology · 2025Review
- Disrupting USP39 deubiquitinase function impairs the survival and migration of multiple myeloma cells through ZEB1 degradation.Journal of experimental & clinical cancer research : CR · 2024Article
- Knockdown of SLC39A14 inhibits glioma progression by promoting erastin-induced ferroptosis SLC39A14 knockdown inhibits glioma progression.BMC cancer · 2023Article
- Integration of clinical characteristics and molecular signatures of the tumor microenvironment to predict the prognosis of neuroblastoma.Journal of molecular medicine (Berlin, Germany) · 2023Article
- USP39 promotes hepatocellular carcinogenesis through regulating alternative splicing in cooperation with SRSF6/HNRNPC.Cell death & disease · 2023Article
- USP39-mediated deubiquitination of Cyclin B1 promotes tumor cell proliferation and glioma progression.Translational oncology · 2023Article
- USP39 stabilizes β-catenin by deubiquitination and suppressing E3 ligase TRIM26 pre-mRNA maturation to promote HCC progression.Cell death & disease · 2023Article
- Underlying mechanisms and clinical potential of circRNAs in glioblastoma.Oncology research · 2023Review
- Unraveling the transcriptomic signatures of Parkinson's disease and major depression using single-cell and bulk data.Frontiers in aging neuroscience · 2023Article
- Review
- The Deubiquitinase USP39 Promotes Esophageal Squamous Cell Carcinoma Malignancy as a Splicing Factor.Genes · 2022Article
- Targeting the splicing factor NONO inhibits GBM progression through GPX1 intron retention.Theranostics · 2022Article
- Ubiquitin-specific peptidase 39 promotes human glioma cells migration and invasion by facilitating ADAM9 mRNA maturation.Molecular oncology · 2022Article
- LINC00520: A Potential Diagnostic and Prognostic Biomarker in Cancer.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing evidence demonstrates that ubiquitin specific protease 39 (USP39) plays an oncogenic role in various human tumors. Here, using expression analysis of the publicly available Oncomine database, clinical glioma patient samples, and glioma cells, we found that USP39 was overexpressed in human gliomas. Knockdown of USP39 in glioma cells demonstrated that the protein promoted cell growth, invasion and migration in vitro and in a tumor model in nude mice. To identify mediators of USP39 growth-promoting properties, we used luciferase reporter constructs under transcriptional control of various promoters specific to seven canonical cancer-associated pathways. Luciferase activity from a synthetic TEAD-dependent YAP/TAZ-responsive reporter, as a direct readout of the Hippo signaling pathway, was decreased by 92% in cells with USP39 knockdown, whereas the luciferase activities from the other six cancer pathways, including MAPK/ERK, MAPK/JNK, NFκB, Notch, TGFβ, and Wnt, remained unchanged. TAZ protein expression however was decreased independent of canonical Hippo signaling. Immunohistochemistry revealed a positive correlation between USP39 and TAZ proteins in orthotopic xenografts derived from modified glioma cells expressing USP39 shRNAs and primary human glioma samples (p < 0.05). Finally, loss of USP39 decreased TAZ pre-mRNA splicing efficiency in glioma cells in vitro, which led to reduced levels of TAZ protein. In summary, USP39 has oncogenic properties that increase TAZ protein levels by inducing maturation of its mRNA. USP39 therefore provides a novel therapeutic target for the treatment of human glioma.
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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.