ArticleInternational journal of molecular sciences2020
GOLPH3 Regulates EGFR in T98G Glioblastoma Cells by Modulating Its Glycosylation and Ubiquitylation.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Clinicopathologic and prognostic implications of Golgi Phosphoprotein 3 in colorectal cancer: A meta-analysis.PloS one · 2021Pooled it
- GOLPH3-mediated sialylation of CXCR4 drives malignant progression and M2 macrophage polarization in colorectal cancer.Apoptosis : an international journal on programmed cell death · 2026Article
- Intestinal Fucosylation: A Key Regulatory Hub in Homeostasis and Disease Pathogenesis.Biomolecules · 2026Review
- Cadmium impairs heart ventricular formation and disrupts polysialylated-NCAM/FGF receptor signaling in Xenopus tadpoles.Cell & bioscience · 2026Article
- Effects of N361 Glycosylation on Epidermal Growth Factor Receptor Biological Function.Cancers · 2026Article
- A novel prognostic model based on Golgi apparatus-related genes predicts patient survival in glioblastoma.Open medicine (Warsaw, Poland) · 2026Article
- The link between the trans-Golgi network and tumour progression.Molecular biology reports · 2025Review
- Golgicide A induces pyroptosis of lung cancer stem cells by regulating dTGN formation via GOLPH3/MYO18A complex.Stem cell research & therapy · 2025Article
- ARMH3 is an ARL5 effector that promotes PI4KB-catalyzed PI4P synthesis at the trans-Golgi network.Nature communications · 2024Article
- Biochemical Pathways Delivering Distinct Glycosphingolipid Patterns in MDA-MB-231 and MCF-7 Breast Cancer Cells.Current issues in molecular biology · 2024Review
- Article
- Sialylation of EGFR by ST6GAL1 induces receptor activation and modulates trafficking dynamics.bioRxiv : the preprint server for biology · 2023Article
- Abnormal glycosylation in glioma: related changes in biology, biomarkers and targeted therapy.Biomarker research · 2023Review
- Golgi Phosphoprotein 3 Regulates the Physical Association of Glycolipid Glycosyltransferases.International journal of molecular sciences · 2022Article
- Fucosylation in Urological Cancers.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Protein trafficking is altered when normal cells acquire a tumor phenotype. A key subcellular compartment in regulating protein trafficking is the Golgi apparatus, but its role in carcinogenesis is still not well defined. Golgi phosphoprotein 3 (GOLPH3), a peripheral membrane protein mostly localized at the trans-Golgi network, is overexpressed in several tumor types including glioblastoma multiforme (GBM), the most lethal primary brain tumor. Moreover, GOLPH3 is currently considered an oncoprotein, however its precise function in GBM is not fully understood. Here, we analyzed in T98G cells of GBM, which express high levels of epidermal growth factor receptor (EGFR), the effect of stable RNAi-mediated knockdown of GOLPH3. We found that silencing GOLPH3 caused a significant reduction in the proliferation of T98G cells and an unexpected increase in total EGFR levels, even at the cell surface, which was however less prone to ligand-induced autophosphorylation. Furthermore, silencing GOLPH3 decreased EGFR sialylation and fucosylation, which correlated with delayed ligand-induced EGFR downregulation and its accumulation at endo-lysosomal compartments. Finally, we found that EGF failed at promoting EGFR ubiquitylation when the levels of GOLPH3 were reduced. Altogether, our results show that GOLPH3 in T98G cells regulates the endocytic trafficking and activation of EGFR likely by affecting its extent of glycosylation and ubiquitylation.
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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.