ArticleOncotarget2017
Overexpression of ubiquitin specific proteases 44 promotes the malignancy of glioma by stabilizing tumor-promoter securin.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Hypermethylated USP44 deubiquitinates SENP2: a critical mechanism in esophageal cancer progression and a new target for intervention.Clinical epigenetics · 2025Article
- The anti-aging Klotho protects glioblastoma macrophages from radiotherapy-induced inflammation and predicts immunotherapy response.International journal of cancer · 2025Article
- USP44 Overexpression Drives a MYC-Like Gene Expression Program in Neuroblastoma through Epigenetic Reprogramming.Molecular cancer research : MCR · 2024Article
- Deubiquitylating Enzymes in Cancer and Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- Article
- Insight into the physiological and pathological roles of USP44, a potential tumor target (Review).Oncology letters · 2022Review
- USP44 accelerates the growth of T-cell acute lymphoblastic leukemia through interacting with WDR5 and repressing its ubiquitination.International journal of medical sciences · 2022Article
- The Role of the Ubiquitin Proteasome System in Glioma: Analysis Emphasizing the Main Molecular Players and Therapeutic Strategies Identified in Glioblastoma Multiforme.Molecular neurobiology · 2021Review
- The deubiquitinase USP44 promotes Treg function during inflammation by preventing FOXP3 degradation.EMBO reports · 2020Article
- USP44 suppresses proliferation and enhances apoptosis in colorectal cancer cells by inactivating the Wnt/β-catenin pathway via Axin1 deubiquitination.Cell biology international · 2020Article
- Novel prognostic prediction model constructed through machine learning on the basis of methylation-driven genes in kidney renal clear cell carcinoma.Bioscience reports · 2020Article
- Ubiquitin-specific protease-44 inhibits the proliferation and migration of cells via inhibition of JNK pathway in clear cell renal cell carcinoma.BMC cancer · 2020Article
- USP19 Enhances MMP2/MMP9-Mediated Tumorigenesis in Gastric Cancer.OncoTargets and therapy · 2020Article
- Ubiquitin-specific protease 44 inhibits cell growth by suppressing AKT signaling in non-small cell lung cancer.The Kaohsiung journal of medical sciences · 2019Article
- Review
- USP44 Promotes the Tumorigenesis of Prostate Cancer Cells through EZH2 Protein Stabilization.Molecules and cells · 2019Article
- USP44 suppresses pancreatic cancer progression and overcomes gemcitabine resistance by deubiquitinating FBP1.American journal of cancer research · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ubiquitin specific peptidase 44 (USP44) has been identified as an important component of spindle assemble checkpoint (SAC) to prevent the formation of aneuploidy. However, recent study raised a controversy about the effect of USP44 in tumor. Here, we first confirmed the intranuclear localization of USP44 by testing several specific antibodies to recognize endogenous USP44. Then, data from IHC and qRT-PCR assay indicated that the high expression of USP44 existed in high-grade glioma tissues and signified a poor prognosis. Knockdown of USP44 inhibited proliferation, migration and invasion, induced apoptosis, and arrested cell cycle in G2/M phase in the established glioma cell lines. Down-regulation of oncoprotein securin was detected in USP44 deficient cells, and the interaction of endogenous USP44 and securin was confirmed by immunoprecipitation in U251MG cells, which indicated that securin was a substrate of USP44, and might be stabilized by USP44.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.