ArticleJournal of experimental & clinical cancer research : CR2009
Transcription factor Sp1 induces ADAM17 and contributes to tumor cell invasiveness under hypoxia.
Article in Journal of experimental & clinical cancer research : CR, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 60 citations in OpenAlex.
- The ADAM Family of Proteases: Structure, Substrates, and Roles in Liver Diseases.International journal of molecular sciences · 2026Review
- Modeling Glioblastoma with Brain Organoids: New Frontiers in Oncology and Space Research.International journal of molecular sciences · 2025Review
- SP1 promotes triple-negative breast cancer progression by targeting USP5.Cancer cell international · 2025Article
- Chronic intermittent hypoxia facilitates the development of angiotensin II-induced abdominal aortic aneurysm in male mice.Journal of applied physiology (Bethesda, Md. : 1985) · 2024Article
- TRIM56 acts through the IQGAP1-CDC42 signaling axis to promote glioma cell migration and invasion.Cell death & disease · 2023Article
- The Orphan GPR50 Receptor Regulates the Aggressiveness of Breast Cancer Stem-like Cells via Targeting the NF-kB Signaling Pathway.International journal of molecular sciences · 2023Article
- ADAM10 mediates shedding of carbonic anhydrase IX ectodomain non‑redundantly to ADAM17.Oncology reports · 2023Article
- SP and KLF Transcription Factors in Cancer Metabolism.International journal of molecular sciences · 2022Review
- Sp1 induced gene TIMP1 is related to immune cell infiltration in glioblastoma.Scientific reports · 2022Article
- Immunomodulatory role of metalloproteinase ADAM17 in tumor development.Frontiers in immunology · 2022Review
- ADAMDEC1 accelerates GBM progressionFrontiers in oncology · 2022Article
- The HIF target MAFF promotes tumor invasion and metastasis through IL11 and STAT3 signaling.Nature communications · 2021Article
- Implications of ADAM17 activation for hyperglycaemia, obesity and type 2 diabetes.Bioscience reports · 2021Review
- Hypoxia-inducible factor-dependent ADAM12 expression mediates breast cancer invasion and metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- GPR50 Promotes Hepatocellular Carcinoma Progression via the Notch Signaling Pathway through Direct Interaction with ADAM17.Molecular therapy oncolytics · 2020Article
- Fractalkine/CX3CL1 in Neoplastic Processes.International journal of molecular sciences · 2020Review
- Caspr1 Facilitates sAPPα Production by Regulating α-Secretase ADAM9 in Brain Endothelial Cells.Frontiers in molecular neuroscience · 2020Article
- The role of NF-κB and Elk-1 in the regulation of mouse ADAM17 expression.Biology open · 2019Article
- MiRNA-130a-3p inhibits cell proliferation, migration, and TMZ resistance in glioblastoma by targeting Sp1.American journal of translational research · 2019Article
- Long non-coding RNA CASC15 regulates gastric cancer cell proliferation, migration and epithelial mesenchymal transition by targeting CDKN1A and ZEB1.Molecular oncology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundExpression of the Sp1 transcription factor is induced by hypoxia, and the ADAM17 promoter contains predicted Sp1 binding sites. ADAM17 contributes to hypoxic-induce invasiveness of glioma. In this study, we investigated whether Sp1 transcription factor induces ADAM17 and/or contributes to tumor cell invasiveness in hypoxia.
methodsEmploying RT-PCR and Western blot, we examined the role of Sp1 in ADAM17 transcription/expression under normoxic and hypoxic conditions, and whether it binds to the ADAM17 GC-rich promoter region using a chromatin immunoprecipitation assay. Additionally, we tested the effect of Sp1 suppression in tumor cell invasion and migration, using Matrigel basement membrane invasion chambers, a scratch wound-healing assay, and small interfering RNA.
resultsHere, we found that Sp1 binds to the ADAM17 promoter, and that Sp1 regulates ADAM17 expression under hypoxia. Furthermore, suppression of Sp1 decreases invasiveness and migration in U87 tumor cells.
conclusionOur findings suggest the Sp1 transcription factor mediates ADAM17 expression under hypoxia, regulates glioma invasiveness, and thus, may be a target for anti-invasion therapies.
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.