ArticleBiology direct2024
DTX2 promotes glioma development via regulation of HLTF.
Article in Biology direct, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 3 citations in OpenAlex.
- Deltex 2 Mediates Oxidative Stress and Neurotoxicity in Freezing of Gait of Parkinson's Disease via the Notch2-Nrf2 Axis.CNS neuroscience & therapeutics · 2026Article
- A Novel Role of DELTEX2 in Maintaining Genomic Stability of Granulosa Cells During Ovarian Aging.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- DTX3 inhibits cell migration, invasion, and epithelial-mesenchymal transition in colorectal cancer through the AKT signaling pathway.Translational cancer research · 2025Article
- [High expression of DTX2 promotes proliferation, invasion and epithelial-mesenchymal transition of oxaliplatin-resistant colorectal cancer cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Therapeutic effects of paeonol on non‑small cell lung cancer cells via regulation of the MAPK pathway.Oncology letters · 2024Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundHuman Deltex 2 (DTX2) is a ubiquitin E3 ligase that functions as an oncogene and has been shown to participate in many human cancers. However, the role of DTX2 in glioma progression has remained obscure. In this study, we explore the mechanism underlying the function of DTX2 in glioma progression.
methodsThe associations between DTX2 expression and clinical characteristics of glioma were determined by bioinformatic analysis of data from The Cancer Genome Atlas and Human Protein Atlas. The expression of DTX2 in glioma tissues was detected using immunohistochemistry and western blotting. Lentivirus-mediated gene knockdown and overexpression were used to determine the effects of DTX2 and helicase-like transcription element (HLTF) on glioma cell proliferation and migration with CCK-8, cell colony formation, transwell, and wound healing assays; flow cytometry in vitro; and animal models in vivo. The interaction of the DTX2 and HLTF proteins was verified by immunoprecipitation assay and confocal microscopy.
resultsDTX2 was highly expressed in glioma samples, and this was correlated with worse overall survival. Silencing of DTX2 suppressed glioma cell viability, colony formation, and migration and induced cell apoptosis. In vitro ubiquitination assays confirmed that DTX2 could downregulate HLTF protein levels by increasing ubiquitination of the HLTF protein. We also observed that HLTF inhibited proliferation and migration of glioma cells. Subcutaneous xenografts with DTX2-overexpressing U87 cells showed significantly increased tumor volumes and weights.
conclusionsWe have identified DTX2/HLTF as a new axis in the development of glioma that could serve as a prognostic or therapeutic marker.
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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 OpenQuestion graph.