ArticleOncogene2021
Metastasis-suppressor NME1 controls the invasive switch of breast cancer by regulating MT1-MMP surface clearance.
Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Monodisperse Chemical Oligophosphorylation of Peptides via Protected Oligophosphorimidazolide Reagents.Angewandte Chemie (International ed. in English) · 2025Article
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- Hsa_circ_ROBO1 competes with miR-324-3p and upregulates NME1 to promote tumor metastasis in nasopharyngeal carcinoma.Discover oncology · 2024Article
- Histidine Phosphorylation: Protein Kinases and Phosphatases.International journal of molecular sciences · 2024Review
- NucleariScience · 2024Article
- Therapeutic potential of Phycocyanin in gastrointestinal cancers and related disorders.Molecular biology reports · 2024Review
- Recent progress in Surface-Enhanced Raman Spectroscopy detection of biomarkers in liquid biopsy for breast cancer.Frontiers in oncology · 2024Review
- Mechanisms of action of NME metastasis suppressors - a family affair.Cancer metastasis reviews · 2023Review
- A perspective on the metastasis suppressor field.Cancer metastasis reviews · 2023Review
- MT1-MMP as a Key Regulator of Metastasis.Cells · 2023Review
- Glaucoma-Associated CDR1 Peptide Promotes RGC Survival in Retinal Explants through Molecular Interaction with Acidic Leucine Rich Nuclear Phosphoprotein 32A (ANP32A).Biomolecules · 2023Article
- MCL1 Inhibition Overcomes the Aggressiveness Features of Triple-Negative Breast Cancer MDA-MB-231 Cells.International journal of molecular sciences · 2023Article
- Multiscale model of the different modes of cancer cell invasion.Bioinformatics (Oxford, England) · 2023Article
- Viscoelastic hydrogels for interrogating pancreatic cancer-stromal cell interactions.Materials today. Bio · 2023Article
- Nano-Based Drug Delivery of Polyphenolic Compounds for Cancer Treatment: Progress, Opportunities, and Challenges.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Molecular interaction of metastasis suppressor genes and tumor microenvironment in breast cancer.Exploration of targeted anti-tumor therapy · 2023Review
- ATP and Adenosine Metabolism in Cancer: Exploitation for Therapeutic Gain.Pharmacological reviews · 2022Review
- DNA damage repair-related gene signature predicts prognosis and indicates immune cell infiltration landscape in skin cutaneous melanoma.Frontiers in endocrinology · 2022Article
- Surface tension of model tissues during malignant transformation and epithelial-mesenchymal transition.Frontiers in cell and developmental biology · 2022Article
- A Journey on Extracellular Vesicles for Matrix Metalloproteinases: A Mechanistic Perspective.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
18 authors at 7 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Membrane Type 1 Matrix Metalloprotease (MT1-MMP) contributes to the invasive progression of breast cancers by degrading extracellular matrix tissues. Nucleoside diphosphate kinase, NME1/NM23-H1, has been identified as a metastasis suppressor; however, its contribution to local invasion in breast cancer is not known. Here, we report that NME1 is up-regulated in ductal carcinoma in situ (DCIS) as compared to normal breast epithelial tissues. NME1 levels drop in microinvasive and invasive components of breast tumor cells relative to synchronous DCIS foci. We find a strong anti-correlation between NME1 and plasma membrane MT1-MMP levels in the invasive components of breast tumors, particularly in aggressive histological grade III and triple-negative breast cancers. Knockout of NME1 accelerates the invasive transition of breast tumors in the intraductal xenograft model. At the mechanistic level, we find that MT1-MMP, NME1 and dynamin-2, a GTPase known to require GTP production by NME1 for its membrane fission activity in the endocytic pathway, interact in clathrin-coated vesicles at the plasma membrane. Loss of NME1 function increases MT1-MMP surface levels by inhibiting endocytic clearance. As a consequence, the ECM degradation and invasive potentials of breast cancer cells are enhanced. This study identifies the down-modulation of NME1 as a potent driver of the in situ-to invasive transition during breast cancer progression.
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