ArticlePloS one2018
DSE promotes aggressive glioma cell phenotypes by enhancing HB-EGF/ErbB signaling.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
- The brain imaging feature-related gene NRP2 drives the malignant progression of glioblastoma through the FAK pathway: a Mendelian randomization study.Translational oncology · 2026Article
- Causal Associations of Heparin-Binding Growth and Differentiation Factors With Thyroid Cancer: A Two-Sample Mendelian Randomization Study.International journal of endocrinology · 2026Article
- Identification and validation of a metabolism-related gene signature for predicting the prognosis of paediatric medulloblastoma.Scientific reports · 2024Article
- DSE inhibits melanoma progression by regulating tumor immune cell infiltration and VCAN.Cell death discovery · 2023Article
- CHST11-modified chondroitin 4-sulfate as a potential therapeutic target for glioblastoma.American journal of cancer research · 2023Article
- Proteoglycans: a common portal for SARS-CoV-2 and extracellular vesicle uptake.American journal of physiology. Cell physiology · 2023Review
- Identifying common transcriptome signatures of cancer by interpreting deep learning models.Genome biology · 2022Article
- Long non-coding RNA TFAP2A-AS1 plays an important role in oral squamous cell carcinoma: research includes bioinformatics analysis and experiments.BMC oral health · 2022Article
- Glycomaterials to Investigate the Functional Role of Aberrant Glycosylation in Glioblastoma.Advanced healthcare materials · 2022Review
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- Comprehensive omics analyses profile genesets related with tumor heterogeneity of multifocal glioblastomas and reveal LIF/CCL2 as biomarkers for mesenchymal subtype.Theranostics · 2022Article
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- Systematic analysis of migration factors by MigExpress identifies essential cell migration control genes in non-small cell lung cancer.Molecular oncology · 2021Article
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- The structure of human dermatan sulfate epimerase 1 emphasizes the importance of C5-epimerization of glucuronic acid in higher organisms.Chemical science · 2021Article
- Upregulated proteoglycan-related signaling pathways in fluid flow shear stress-treated podocytes.American journal of physiology. Renal physiology · 2020Article
- Chondroitin sulfate synthase 1 enhances proliferation of glioblastoma by modulating PDGFRA stability.Oncogenesis · 2020Article
- Proteoglycans as Therapeutic Targets in Brain Cancer.Frontiers in oncology · 2020Review
- The dual role of the glycosaminoglycan chondroitin-6-sulfate in the development, progression and metastasis of cancer.The FEBS journal · 2019Review
- A Robust Gene Expression Prognostic Signature for Overall Survival in High-Grade Serous Ovarian Cancer.Journal of oncology · 2019Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Remodeling of the extracellular matrix (ECM) in the tumor microenvironment promotes glioma progression. Chondroitin sulfate (CS) proteoglycans appear in the ECM and on the cell surface, and can be catalyzed by dermatan sulfate epimerase to form chondroitin sulfate/dermatan sulfate (CS/DS) hybrid chains. Dermatan sulfate epimerase 1 (DSE) is overexpressed in many types of cancer, and CS/DS chains mediate several growth factor signals. However, the role of DSE in gliomas has never been explored. In the present study, we determined the expression of DSE in gliomas by consulting a public database and conducting immunohistochemistry on a tissue array. Our investigation revealed that DSE was upregulated in gliomas compared with normal brain tissue. Furthermore, high DSE expression was associated with advanced tumor grade and poor survival. We found high DSE expression in several glioblastoma cell lines, and DSE expression directly mediated DS chain formation in glioblastoma cells. Knockdown of DSE suppressed the proliferation, migration, and invasion of glioblastoma cells. In contrast, overexpression of DSE in GL261 cells enhanced these malignant phenotypes and in vivo tumor growth. Interestingly, we found that DSE selectively regulated heparin-binding EGF-like growth factor (HB-EGF)-induced signaling in glioblastoma cells. Inhibiting epidermal growth factor receptor (EGFR) and ErbB2 with afatinib suppressed DSE-enhanced malignant phenotypes, establishing the critical role of the ErbB pathway in regulating the effects of DSE expression. This evidence indicates that upregulation of DSE in gliomas contributes to malignant behavior in cancer cells. We provide novel insight into the significance of DS chains in ErbB signaling and glioma pathogenesis.
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