ArticlePharmacological reports : PR2026
CC8, a heterodimeric disintegrin from Cerastes cerastes snake venom, triggers apoptosis and restrains the dissemination of human glioblastoma cells.
Article in Pharmacological reports : PR, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlioblastoma (GBM) is the most aggressive and frequent primary malignant brain tumor and remains highly resistant to existing therapies. Snake-venom disintegrins possess potent anticancer activities, yet their pharmacological potential against GBM is not fully explored. In this work, we aimed to evaluate the therapeutic potential of the disintegrin CC8 from Cerastes cerastes snake venom, toward the development of a novel anti-GBM drug.
methodsThe effects of CC8 on the viability and proliferation of human GBM cell lines U87, U251, LN229, and LN18 were assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and crystal violet assays. Apoptosis induction was examined by annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) staining and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis of pro- and anti-apoptotic gene expression. The effect of CC8 on cell-extracellular matrix (ECM) interactions was evaluated through adhesion assays and integrin-blocking antibodies. GBM cell infiltration potential was further explored using cell invasion assays and spheroid-based migration models.
resultsCC8 significantly reduced the viability of U87, LN18, and LN229 cells and inhibited the proliferation of U87, whereas U251 cells showed resistance up to 200 nM. CC8 induced caspase-dependent apoptosis, as evidenced by downregulation of BCL2 apoptosis regulator (BCL2) and upregulation of BCL2-associated X, apoptosis regulator (BAX), caspase 3 (CASP3), and caspase 8 (CASP8) expression. CC8 also disrupted cell adhesion to fibrinogen (Fg) and fibronectin (Fn) through integrin interference. Furthermore, it markedly decreased GBM cell invasion and reduced U87 spheroid migration.
conclusionsThese findings identify CC8 as a promising venom-derived candidate for GBM drug development, with potential to improve therapeutic outcomes for this aggressive and treatment-resistant cancer. CLINICAL TRIAL NUMBER: Not applicable.
Indexed as
Identifiers
41811660What 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.