ArticleThe Journal of clinical investigation2017
Epithelial-to-mesenchymal transition drives a pro-metastatic Golgi compaction process through scaffolding protein PAQR11.
Article in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
70 citing papers in PubMed, 105 citations in OpenAlex.
- PAQR11: An evolutionarily conserved Golgi receptor governing metabolic-immune crosstalk and systemic homeostasis.Histology and histopathology · 2026Review
- Identification of a novel signature for prognostic stratification and integrative analyses in lung adenocarcinoma.Translational cancer research · 2026Article
- EMT activates ER-to-Golgi trafficking through upregulation of REEP2 to promote lung cancer progression.Research square · 2026Article
- Fam3C alters Golgi apparatus morphology and function in triple negative breast cancer.Journal of molecular cell biology · 2026Article
- Osimertinib activates a TGF-β2-dependent secretory program that drives lung adenocarcinoma progression.The Journal of clinical investigation · 2026Article
- Golgi Drivers of Cancer.Sub-cellular biochemistry · 2026Review
- The Impact of Golgi Organization on Cell Cycle and Cancer Development.Sub-cellular biochemistry · 2026Review
- EMT activates ER-to-Golgi trafficking through upregulation of REEP2 to promote lung cancer progression.bioRxiv : the preprint server for biology · 2025Article
- A morphology-based machine learning model for scoring epithelial-mesenchymal plasticity using organelle dynamics.Communications biology · 2025Article
- Complimentary vertebratebioRxiv : the preprint server for biology · 2025Article
- Monensin suppresses EMT-driven cancer cell motility by inducing Golgi pH-dependent exocytosis of GOLIM4.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Dichotomous roles of ACBD3 in NSCLC growth and metastasis.Oncogene · 2025Article
- Hyaluronan network remodeling by ZEB1 and ITIH2 enhances the motility and invasiveness of cancer cells.The Journal of clinical investigation · 2025Article
- Multi-omics pan-cancer analysis of monocyte to macrophage differentiation-associated (MMD) and its significance in hepatocellular carcinoma.Cancer biomarkers : section A of Disease markers · 2025Article
- Opsin3 regulates cell proliferation, migration, and apoptosis in lung adenocarcinoma via GPX3 pathway.European journal of medical research · 2025Article
- Review
- The cancer-associated secretory phenotype: a new frontier in targeted therapeutics.The Journal of clinical investigation · 2024Review
- Review
- Article
- Quaking isoforms cooperate to promote the mesenchymal phenotype.Molecular biology of the cell · 2024Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 7 institutions in 4 countries.
Funding
Abstract
Tumor cells gain metastatic capacity through a Golgi phosphoprotein 3-dependent (GOLPH3-dependent) Golgi membrane dispersal process that drives the budding and transport of secretory vesicles. Whether Golgi dispersal underlies the pro-metastatic vesicular trafficking that is associated with epithelial-to-mesenchymal transition (EMT) remains unclear. Here, we have shown that, rather than causing Golgi dispersal, EMT led to the formation of compact Golgi organelles with improved ribbon linking and cisternal stacking. Ectopic expression of the EMT-activating transcription factor ZEB1 stimulated Golgi compaction and relieved microRNA-mediated repression of the Golgi scaffolding protein PAQR11. Depletion of PAQR11 dispersed Golgi organelles and impaired anterograde vesicle transport to the plasma membrane as well as retrograde vesicle tethering to the Golgi. The N-terminal scaffolding domain of PAQR11 was associated with key regulators of Golgi compaction and vesicle transport in pull-down assays and was required to reconstitute Golgi compaction in PAQR11-deficient tumor cells. Finally, high PAQR11 levels were correlated with EMT and shorter survival in human cancers, and PAQR11 was found to be essential for tumor cell migration and metastasis in EMT-driven lung adenocarcinoma models. We conclude that EMT initiates a PAQR11-mediated Golgi compaction process that drives metastasis.
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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.