ArticleJournal of experimental & clinical cancer research : CR2008
Cilengitide induces cellular detachment and apoptosis in endothelial and glioma cells mediated by inhibition of FAK/src/AKT pathway.
Article in Journal of experimental & clinical cancer research : CR, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed, 111 citations in OpenAlex.
- Phase II study of cilengitide (EMD 121974, NSC 707544) in patients with non-metastatic castration resistant prostate cancer, NCI-6735. A study by the DOD/PCF prostate cancer clinical trials consortium.Investigational new drugs · 2012Trial
- The intersection of chemokine signaling with the hallmarks of cancer in glioblastoma.Journal of neuro-oncology · 2026Review
- Integrin inhibition differentially remodels vascular networks in lung metastases driven by vessel co-option or angiogenesis.Angiogenesis · 2026Article
- Design and Verification Process of a Structure-Altering Peptide as a Microtubule Allosteric Polypeptide Against Cancer.The protein journal · 2025Article
- Thyroid hormones contribute to JAK/STAT pathway abnormal activation, promoting T-cell lymphoma dissemination.Blood advances · 2025Article
- K562 Chronic Myeloid Leukemia Cells as a Dual β3-Expressing Functional Cell Line Model to Investigate the Effects of Combined αIIbβ3 and αvβ3 Antagonism.Methods and protocols · 2025Article
- Cartilage Oligomeric Matrix Protein Promotes Radiation Resistance in Non-Small Cell Lung Cancer In Vitro.International journal of molecular sciences · 2025Article
- Targeting stromal cells in tumor microenvironment as a novel treatment strategy for glioma.Cancer cell international · 2025Review
- Targeted inhibition of integrin αVβ3 induces cytotoxicity and suppresses migration ability in ovarian cancer cells and tumor spheroids.International journal of medical sciences · 2025Article
- Deciphering the Tumor Microenvironment in Prostate Cancer: A Focus on the Stromal Component.Cancers · 2024Review
- Roles for epithelial integrin α3β1 in regulation of the microenvironment during normal and pathological tissue remodeling.American journal of physiology. Cell physiology · 2024Review
- The Potential Role of the Extracellular Matrix Glycoprotein Reelin in Glioblastoma Biology.Pharmaceuticals (Basel, Switzerland) · 2024Article
- A novel class of inhibitors that disrupts the stability of integrin heterodimers identified by CRISPR-tiling-instructed genetic screens.Nature structural & molecular biology · 2024Article
- Article
- Sandwich Culture Platforms to Investigate the Roles of Stiffness Gradients and Cell-Matrix Adhesions in Cancer Cell Migration.Cancers · 2023Article
- The complex relationship between integrins and oncolytic herpes Simplex Virus 1 in high-grade glioma therapeutics.Molecular therapy oncolytics · 2022Review
- Cilengitide, an αvβ3-integrin inhibitor, enhances the efficacy of anti-programmed cell death-1 therapy in a murine melanoma model.Bioengineered · 2022Article
- Cilengitide Inhibits Neovascularization in a Rabbit Abdominal Aortic Plaque Model by Impairing the VEGF Signaling.BioMed research international · 2021Article
- EDIL3 promotes epithelial-mesenchymal transition and paclitaxel resistance through its interaction with integrin αCell death discovery · 2020Article
- Antitumor activity of integrin αTranslational cancer research · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe antiangiogenic agent cilengitide disrupts integrin binding to the extracellular matrix leading to apoptosis of activated endothelial cells. Integrins are also widely expressed in malignant glioma and integrin inhibitors may directly target tumor cells in this disease. Aim of the current study was to investigate effects of cilengitide on endothelial and glioma cells on molecular and cellular levels.
resultsCilengitide caused dose-dependent detachment of endothelial cells from cell culture dishes. Proliferation of endothelial cells was significantly inhibited while the proportion of apoptotic cells was increased. Incubation of integrin-expressing glioma cells with cilengitide caused rounding and detachment after 24 hours as observed with endothelial cells. Cilengitide inhibited proliferation and induced apoptosis in glioma cells with methylated MGMT promotor when given alone or in combination with temozolomide. In endothelial as well as glioma cells cilengitide inhibited phosphorylation of FAK, Src and Akt. Assembly of cytoskeleton and tight junctions was heavily disturbed in both cell types.
conclusionCilengitide inhibits integrin-dependent signaling, causes disassembly of cytoskeleton, cellular detachment and induction of apoptosis in endothelial and glioma cells thereby explaining the profound activity of integrin inhibitors in gliomas. The combination of cilengitide with temozolomide exerted additive effects in glioma cells as observed clinically.
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.