ArticleNature communications2024
Intercellular transfer of cancer cell invasiveness via endosome-mediated protease shedding.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 25 citations in OpenAlex.
- Differential expression of TKS4 isoforms and their role in cellular processes in breast cancer.Journal of cell communication and signaling · 2026Article
- Interaction of HS1BP3 with cortactin modulates TKS5 localisation, cell secretion and cancer malignancy.Molecular oncology · 2026Article
- Molecular subtyping and prognostic model construction based on endosome-related genes in colorectal cancer.Journal of gastrointestinal oncology · 2026Article
- Engineered T cell membrane coated nanoparticles reverse thermo-resistance and reprogram tumor microenvironment to synergistically potentiate bladder cancer photothermal immunotherapy.Journal of nanobiotechnology · 2026Article
- Amoeboid-mesenchymal transition and the proteolytic control of cancer invasion plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- Multi-center multi-omics integration predicts individualized prognosis in medullary thyroid carcinoma.Nature communications · 2026Article
- Porcine cells restrict human cell proliferation via cellular competition in a human-porcine mesenchymal stem cells co-culture model.Frontiers in cell and developmental biology · 2026Article
- A pretreatment 15-gene signature predicts non-pCR in response to neoadjuvant chemotherapy in breast cancer and reveals a pyruvate-Frontiers in oncology · 2026Article
- Epigenetic drivers of metalloproteinases and metastasis.Trends in cell biology · 2025Review
- A review on the role of IL-6 in the onset and progression of nasopharyngeal carcinoma.Medical oncology (Northwood, London, England) · 2025Review
- Chemoselective Characterization of New Extracellular Matrix Deposition in Bioengineered Tumor Tissues.Advanced materials (Deerfield Beach, Fla.) · 2025Article
- LncRNA-like MMP14 RNA facilitates colorectal cancer metastasis by suppressing H3K27cr at the STARD13 promoter region.Cellular & molecular biology letters · 2025Article
- Alpha-synuclein modulates the positioning of endolysosomes in melanoma cells.Human molecular genetics · 2025Article
- Tethered Exosomes Containing the Matrix Metalloproteinase MT1-MMP Contribute to Extracellular Matrix Degradation.Journal of extracellular vesicles · 2025Article
- Protease regulation of tumor-immune cell symbiosis.Trends in cancer · 2025Review
- Spatiotemporally resolved mapping of extracellular proteomes via in vivo-compatible TyroID.Nature communications · 2025Article
- Review
- Assessment of Protein Immunoexpression Associated with Tumor Proliferation and Invasion in Histological Subtypes of Unicystic and Conventional Ameloblastoma.International journal of molecular sciences · 2025Article
- Components of the Endosome-Lysosome Vesicular Machinery as Drivers of the Metastatic Cascade in Prostate Cancer.Cancers · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Overexpression of the transmembrane matrix metalloproteinase MT1-MMP/MMP14 promotes cancer cell invasion. Here we show that MT1-MMP-positive cancer cells turn MT1-MMP-negative cells invasive by transferring a soluble catalytic ectodomain of MT1-MMP. Surprisingly, this effect depends on the presence of TKS4 and TKS5 in the donor cell, adaptor proteins previously implicated in invadopodia formation. In endosomes of the donor cell, TKS4/5 promote ADAM-mediated cleavage of MT1-MMP by bridging the two proteases, and cleavage is stimulated by the low intraluminal pH of endosomes. The bridging depends on the PX domains of TKS4/5, which coincidently interact with the cytosolic tail of MT1-MMP and endosomal phosphatidylinositol 3-phosphate. MT1-MMP recruits TKS4/5 into multivesicular endosomes for their subsequent co-secretion in extracellular vesicles, together with the enzymatically active ectodomain. The shed ectodomain converts non-invasive recipient cells into an invasive phenotype. Thus, TKS4/5 promote intercellular transfer of cancer cell invasiveness by facilitating ADAM-mediated shedding of MT1-MMP in acidic endosomes.
Indexed as
Identifiers
What OpenQuestion holds
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.