ArticleThe Journal of biological chemistry2014
An oncogenic protein Golgi phosphoprotein 3 up-regulates cell migration via sialylation.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 3 of them syntheses that pooled it.
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Who cites it
62 citing papers in PubMed, 3 syntheses or guidelines pooled it, 95 citations in OpenAlex.
- Tissue-Based Markers as a Tool to Assess Response to Neoadjuvant Radiotherapy in Rectal Cancer-Systematic Review.International journal of molecular sciences · 2022Pooled it
- Clinicopathologic and prognostic implications of Golgi Phosphoprotein 3 in colorectal cancer: A meta-analysis.PloS one · 2021Pooled it
- Golgi phosphoprotein3 overexpression is associated with poor survival in patients with solid tumors: a meta-analysis.International journal of clinical and experimental pathology · 2015Pooled it
- Oncogenic receptor tyrosine kinase signaling is driven by the Golgi protein GOLPH3 and its interaction with MYO18A.Science signaling · 2026Article
- AXL receptor tyrosine kinase regulates Golgi organization and function via an adhesion-Arf1 signalling axis in breast and lung cancer cell lines.Biology open · 2026Article
- Cadmium impairs heart ventricular formation and disrupts polysialylated-NCAM/FGF receptor signaling in Xenopus tadpoles.Cell & bioscience · 2026Article
- Mining cancer genomes for copy number alterations identifies glycosylation enzymes as oncogenic drivers.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Golgi Drivers of Cancer.Sub-cellular biochemistry · 2026Review
- Metal Ion-Enhanced ZIC-cHILIC StageTip for N-Glycoproteomic and Phosphoproteomic Profiling in EGFR-Mutated Lung Cancer Cells.Molecular & cellular proteomics : MCP · 2025Article
- Review
- Trafficking and localization of Golgi-residentFrontiers in plant science · 2025Review
- GOLPH3 and GOLPH3L maintain Golgi localization of LYSET and a functional mannose 6-phosphate transport pathway.The EMBO journal · 2024Article
- ARMH3 is an ARL5 effector that promotes PI4KB-catalyzed PI4P synthesis at the trans-Golgi network.Nature communications · 2024Article
- Golgiphagy: a novel selective autophagy to the fore.Cell & bioscience · 2024Review
- A UTP3-dependent nucleolar translocation pathway facilitates pre-rRNA 5'ETS processing.Nucleic acids research · 2024Article
- Deciphering the sub-Golgi localization of glycosyltransferases via 3D super-resolution imaging.Cell structure and function · 2024Article
- Specific sialylation of N-glycans and its novel regulatory mechanism.Glycoconjugate journal · 2024Review
- Article
- Stability and function of RCL1 are dependent on the interaction with BMS1.Journal of molecular cell biology · 2024Article
- Role of tumor cell sialylation in pancreatic cancer progression.Advances in cancer research · 2023Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently, the Golgi phosphoprotein 3 (GOLPH3) and its yeast homolog Vps74p have been characterized as essential for the Golgi localization of glycosyltransferase in yeast. GOLPH3 has been identified as a new oncogene that is commonly amplified in human cancers to modulate mammalian target of rapamycin signaling. However, the molecular mechanisms of the carcinogenic signaling pathway remain largely unclear. To investigate whether the expression of GOLPH3 was involved in the glycosylation processes in mammalian cells, and whether it affected cell behavior, we performed a loss-of-function study. Cell migration was suppressed in GOLPH3 knockdown (KD) cells, and the suppression was restored by a re-introduction of the GOLPH3 gene. HPLC and LC/MS analysis showed that the sialylation of N-glycans was specifically decreased in KD cells. The specific interaction between sialyltransferases and GOLPH3 was important for the sialylation. Furthermore, overexpression of α2,6-sialyltransferase-I rescued cell migration and cellular signaling, both of which were blocked in GOLPH3 knockdown cells. These results are the first direct demonstration of the role of GOLPH3 in N-glycosylation to regulate cell biological functions.
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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.