ArticleCancer research2010
Secreted and membrane-bound isoforms of protease ADAM9 have opposing effects on breast cancer cell migration.
Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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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.
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Who cites it
31 citing papers in PubMed, 62 citations in OpenAlex.
- ADAM9: an updated view of its biology and pathology.Molecular biology reports · 2026Review
- ADAM9 in tumor biology: molecular functions, clinical implications, and therapeutic targeting.Cellular & molecular biology letters · 2026Review
- Review
- Unfavorable immunotherapy plus tyrosine kinase inhibition outcome of metastatic renal cell carcinoma after radical nephrectomy with increased ADAM9 expression.Immunogenetics · 2023Article
- Ubiquitin-specific peptidase 39 promotes human glioma cells migration and invasion by facilitating ADAM9 mRNA maturation.Molecular oncology · 2022Article
- Structure, regulatory factors and cancer-related physiological effects of ADAM9.Cell adhesion & migration · 2020Review
- Analysis of ADAM9 regulation and function in vestibular schwannoma primary cells.BMC research notes · 2020Article
- An Overview of ADAM9: Structure, Activation, and Regulation in Human Diseases.International journal of molecular sciences · 2020Review
- ADAM9: A novel player in vestibular schwannoma pathogenesis.Oncology letters · 2020Article
- ADAM9 Mediates Triple-Negative Breast Cancer Progression via AKT/NF-κB Pathway.Frontiers in medicine · 2020Article
- Relationship Between Proteinase with a Disintegrin and a Metalloproteinase Domain-9 (ADAM9), Inflammation, Airway Remodeling, and Emphysema in COPD Patients.International journal of chronic obstructive pulmonary disease · 2020Article
- Identification of the Cell-Surface Protease ADAM9 as an Entry Factor for Encephalomyocarditis Virus.mBio · 2019Article
- The pleiotropic roles of ADAM9 in the biology of solid tumors.Cellular and molecular life sciences : CMLS · 2018Review
- MicroRNA-126 inhibits proliferation and metastasis in prostate cancer via regulation of ADAM9.Oncology letters · 2018Article
- Sorting nexin 9 (SNX9) regulates levels of the transmembrane ADAM9 at the cell surface.The Journal of biological chemistry · 2018Article
- ADAM9 is over-expressed in human ovarian clear cell carcinomas and suppresses cisplatin-induced cell death.Cancer science · 2018Article
- Overexpression of ADAM9 in oral squamous cell carcinoma.Oncology letters · 2018Article
- ADAM9 promotes lung cancer progression through vascular remodeling by VEGFA, ANGPT2, and PLAT.Scientific reports · 2017Article
- Fine Tuning Cell Migration by a Disintegrin and Metalloproteinases.Mediators of inflammation · 2017Review
- ADAM9 Expression Is Associate with Glioma Tumor Grade and Histological Type, and Acts as a Prognostic Factor in Lower-Grade Gliomas.International journal of molecular sciences · 2016Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Tumor cell migration is mediated by cell-autonomous signaling mechanisms as well as paracrine and autocrine factors secreted by activated stromal cells in the tumor microenvironment. Like other members of the ADAM (a disintegrin and metalloproteinase) family, the integrin-binding metalloproteinase ADAM9 modulates cell-cell and cell-matrix interactions as well as ectodomain shedding of cell surface receptors and ligands, thereby modifying intracellular and extracellular signaling. ADAM9 transcripts are alternatively spliced to express a transmembrane protein (ADAM9-L) and a secreted variant (ADAM9-S). In this study, we show that ADAM9-S promotes breast cancer cell migration in a manner requiring its metalloproteinase activity, whereas ADAM9-L suppresses cell migration independent of its metalloproteinase activity. Suppression of migration by ADAM9-L requires a functional disintegrin domain and integrin binding. Expression analysis revealed that both ADAM9 isoforms are expressed in breast cancer cell lines and tissues. Therefore, relative levels of membrane-tethered and secreted variants of ADAM9 are a key determinant in manifestation of aggressive migratory phenotypes associated with breast cancer progression.
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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.