ArticleMolecular biology of the cell2016
GOLPH3 drives cell migration by promoting Golgi reorientation and directional trafficking to the leading edge.
Article in Molecular biology of the cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- Clinicopathologic and prognostic implications of Golgi Phosphoprotein 3 in colorectal cancer: A meta-analysis.PloS one · 2021Pooled it
- Oncogenic receptor tyrosine kinase signaling is driven by the Golgi protein GOLPH3 and its interaction with MYO18A.Science signaling · 2026Article
- Cadmium impairs heart ventricular formation and disrupts polysialylated-NCAM/FGF receptor signaling in Xenopus tadpoles.Cell & bioscience · 2026Article
- Golgi Drivers of Cancer.Sub-cellular biochemistry · 2026Review
- Lipidomics and temporal-spatial distribution of organelle lipid.Journal of biological methods · 2025Review
- Myosin 1e deficiency affects migration of 4T1 breast cancer cells.Cytoskeleton (Hoboken, N.J.) · 2024Article
- Golgi dispersal in cancer stem cells promotes chemoresistance of colorectal cancer via the Golgi stress response.Cell death & disease · 2024Article
- The Golgi Apparatus as an Anticancer Therapeutic Target.Biology · 2023Review
- Unraveling the Intricate Link: Deciphering the Role of the Golgi Apparatus in Breast Cancer Progression.International journal of molecular sciences · 2023Review
- Autoinhibitory mechanism controls binding of centrosomin motif 1 to γ-tubulin ring complex.The Journal of cell biology · 2023Article
- Kinetics of Arf1 inactivation regulates Golgi organisation and function in non-adherent fibroblasts.Biology open · 2023Article
- Actin-driven Golgi apparatus dispersal during collective migration of epithelial cells.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Review
- Persistent cell migration emerges from a coupling between protrusion dynamics and polarized trafficking.eLife · 2022Article
- The core autophagy protein ATG9A controls dynamics of cell protrusions and directed migration.The Journal of cell biology · 2022Article
- Endogenous and Exogenous Regulatory Signaling in the Secretory Pathway: Role of Golgi Signaling Molecules in Cancer.Frontiers in cell and developmental biology · 2022Review
- Cargo sorting at the trans-Golgi network at a glance.Journal of cell science · 2021Article
- A junctional PACSIN2/EHD4/MICAL-L1 complex coordinates VE-cadherin trafficking for endothelial migration and angiogenesis.Nature communications · 2021Article
- The role of the Golgi apparatus in disease (Review).International journal of molecular medicine · 2021Review
- Rab26 suppresses migration and invasion of breast cancer cells through mediating autophagic degradation of phosphorylated Src.Cell death & disease · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The mechanism of directional cell migration remains an important problem, with relevance to cancer invasion and metastasis. GOLPH3 is a common oncogenic driver of human cancers, and is the first oncogene that functions at the Golgi in trafficking to the plasma membrane. Overexpression of GOLPH3 is reported to drive enhanced cell migration. Here we show that the phosphatidylinositol-4-phosphate/GOLPH3/myosin 18A/F-actin pathway that is critical for Golgi-to-plasma membrane trafficking is necessary and limiting for directional cell migration. By linking the Golgi to the actin cytoskeleton, GOLPH3 promotes reorientation of the Golgi toward the leading edge. GOLPH3 also promotes reorientation of lysosomes (but not other organelles) toward the leading edge. However, lysosome function is dispensable for migration and the GOLPH3 dependence of lysosome movement is indirect, via GOLPH3's effect on the Golgi. By driving reorientation of the Golgi to the leading edge and driving forward trafficking, particularly to the leading edge, overexpression of GOLPH3 drives trafficking to the leading edge of the cell, which is functionally important for directional cell migration. Our identification of a novel pathway for Golgi reorientation controlled by GOLPH3 provides new insight into the mechanism of directional cell migration with important implications for understanding GOLPH3's role in cancer.
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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.