ArticleCancer science2007
Inhibition of ADAM17 reduces hypoxia-induced brain tumor cell invasiveness.
Article in Cancer science, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 2 of them syntheses that pooled it.
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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
49 citing papers in PubMed, 2 syntheses or guidelines pooled it, 93 citations in OpenAlex.
- Prognostic Significance of ADAM17 for Gastric Cancer Survival: A Meta-Analysis.Medicina (Kaunas, Lithuania) · 2020Pooled it
- Systematic review of protein biomarkers of invasive behavior in glioblastoma.Molecular neurobiology · 2014Pooled it
- Perturbation of EPHA2 and EFNA1iScience · 2025Article
- MicroRNA-145 in urologic tumors: biological roles, regulatory networks, and clinical translation.Frontiers in pharmacology · 2025Review
- α2,6 Sialylation mediated by ST6GAL1 promotes glioblastoma growth.JCI insight · 2022Article
- Biological implications and clinical potential of invasion and migration related miRNAs in glioma.Frontiers in integrative neuroscience · 2022Review
- Review
- ADAM17 Mediates Hypoxia-Induced Keratinocyte Migration via the p38/MAPK Pathway.BioMed research international · 2021Article
- Fractalkine/CX3CL1 in Neoplastic Processes.International journal of molecular sciences · 2020Review
- Hypoxia-induced release, nuclear translocation, and signaling activity of a DLK1 intracellular fragment in glioma.Oncogene · 2020Article
- Article
- Short hairpin RNA-mediated gene silencing of ADAM17 inhibits the growth of breast cancer MCF‑7 cells in vitro and in vivo and its mechanism of action.Oncology reports · 2018Article
- ADAM10 Sheddase Activity is a Potential Lung-Cancer Biomarker.Journal of Cancer · 2018Article
- Metalloproteinases ADAM10 and ADAM17 Mediate Migration and Differentiation in Glioblastoma Sphere-Forming Cells.Molecular neurobiology · 2017Article
- Therapeutic potential of ADAM17 modulation in gastric cancer through regulation of the EGFR and TNF-α signalling pathways.Molecular and cellular biochemistry · 2017Article
- Modification of proteolytic activity matrix analysis (PrAMA) to measure ADAM10 and ADAM17 sheddase activities in cell and tissue lysates.Journal of Cancer · 2017Article
- Fine Tuning Cell Migration by a Disintegrin and Metalloproteinases.Mediators of inflammation · 2017Review
- Density-Dependent Regulation of Glioma Cell Proliferation and Invasion Mediated by miR-9.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2016Article
- The role of ADAM17 in tumorigenesis and progression of breast cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- Role of ADAM17 in invasion and migration of CD133-expressing liver cancer stem cells after irradiation.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
The membrane-anchored metalloproteinase tumor necrosis factor-alpha-converting enzyme (TACE/a disintegrin and metalloproteinase [ADAM] 17) is key in proteolytic ectodomain shedding of several membrane-bound growth factors, cytokines and receptors. The expression and activity of ADAM17 increases under some pathological conditions including stroke, and promotes neural progenitor cell migration and contributes to stroke-induced neurogenesis. Hypoxia initiates cellular invasive processes that occur under both physiological and pathological conditions such as invasion and metastasis of some tumors. In the present study, we sought to elucidate whether ADAM17 contributes to brain tumor invasion. To this end, we examined the role of ADAM17 in the invasiveness of two different brain tumor cell lines, 9L rat gliosarcoma and U87 human glioma, under normoxic and hypoxic conditions. Additionally, we tested the effects of ADAM17 suppression on in vitro tumor cell invasion by means of ADAM17 proteolytic inhibitors and specific small interfering RNA. We found that tumor cells upregulated ADAM17 expression under hypoxia, and that ADAM17 activity correlated with increased tumor cell invasion. Conversely, suppression of ADAM17 proteolysis decreased invasiveness induced by hypoxia in 9L and U87 cells. Furthermore, the contribution of ADAM17 to tumor invasion was independent of matrix metalloproteinase (MMP)-2 and MMP-9 activity. ADAM17 was also found to activate the epidermal growth factor/phosphoinositide-3 kinase/serine/threonine kinase signal transduction pathway. Our data suggest that hypoxia-induced ADAM17 contributes to glioma cell invasiveness through activation of the EGFR signal pathway.
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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.