ArticleThe Journal of cell biology2020
Protrudin-mediated ER-endosome contact sites promote MT1-MMP exocytosis and cell invasion.
Article in The Journal of cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Stay in touch with the endoplasmic reticulum.Science China. Life sciences · 2024Pooled it
- Interaction of HS1BP3 with cortactin modulates TKS5 localisation, cell secretion and cancer malignancy.Molecular oncology · 2026Article
- Endosomes as central hubs of interorganellar communication and cellular homeostasis.Protein & cell · 2026Review
- Multilayered control of mRNA delivery to cell protrusions drives localized mini-cytoplasm establishment for stress-induced cell activation.Nature communications · 2026Article
- Decoding lactylation heterogeneity in glioblastoma: machine learning identifies G6PC3 as a prognostic target.BMC cancer · 2026Article
- Organelle contact sites in cancer cells.Cell death & disease · 2026Review
- Mechanical observables of cancer invasion: actin, adhesion, and metastatic plasticity.Frontiers in cell and developmental biology · 2026Review
- Tks5 interactome reveals endoplasmic-reticulum-associated translation machinery in invadosomes.The FEBS journal · 2025Article
- Tethered Exosomes Containing the Matrix Metalloproteinase MT1-MMP Contribute to Extracellular Matrix Degradation.Journal of extracellular vesicles · 2025Article
- Invadopodia in cancer metastasis: dynamics, regulation, and targeted therapies.Journal of translational medicine · 2025Review
- Review
- Construction of a prognostic model with exosome biogenesis- and release-related genes and identification of RAB27B in immune infiltration of pancreatic cancer.Translational cancer research · 2024Article
- MCT4 and CD147 colocalize with MMP14 in invadopodia and support matrix degradation and invasion by breast cancer cells.Journal of cell science · 2024Article
- A MAP1B-cortactin-Tks5 axis regulates TNBC invasion and tumorigenesis.The Journal of cell biology · 2024Article
- Intercellular transfer of cancer cell invasiveness via endosome-mediated protease shedding.Nature communications · 2024Article
- Organelle morphology and positioning orchestrate physiological and disease-associated processes.Current opinion in cell biology · 2024Review
- Enhancing drug penetration in solid tumors via nanomedicine: Evaluation models, strategies and perspectives.Bioactive materials · 2024Review
- Fibroblast activation protein drives tumor metastasis via a protease-independent role in invadopodia stabilization.Cell reports · 2023Article
- Long Prehensile Protrusions Can Facilitate Cancer Cell Invasion through the Basement Membrane.Cells · 2023Article
- Protein dynamics at invadopodia control invasion-migration transitions in melanoma cells.Cell death & disease · 2023Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cells break tissue barriers by use of small actin-rich membrane protrusions called invadopodia. Complete invadopodia maturation depends on protrusion outgrowth and the targeted delivery of the matrix metalloproteinase MT1-MMP via endosomal transport by mechanisms that are not known. Here, we show that the ER protein Protrudin orchestrates invadopodia maturation and function. Protrudin formed contact sites with MT1-MMP-positive endosomes that contained the RAB7-binding Kinesin-1 adaptor FYCO1, and depletion of RAB7, FYCO1, or Protrudin inhibited MT1-MMP-dependent extracellular matrix degradation and cancer cell invasion by preventing anterograde translocation and exocytosis of MT1-MMP. Moreover, when endosome translocation or exocytosis was inhibited by depletion of Protrudin or Synaptotagmin VII, respectively, invadopodia were unable to expand and elongate. Conversely, when Protrudin was overexpressed, noncancerous cells developed prominent invadopodia-like protrusions and showed increased matrix degradation and invasion. Thus, Protrudin-mediated ER-endosome contact sites promote cell invasion by facilitating translocation of MT1-MMP-laden endosomes to the plasma membrane, enabling both invadopodia outgrowth and MT1-MMP exocytosis.
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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 Socratic graph.