ArticleAging2024
Bufotalin enhances apoptosis and TMZ chemosensitivity of glioblastoma cells by promoting mitochondrial dysfunction via AKT signaling pathway.
Article in Aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed.
- Natural and Synthetic Compounds, Swords for Glioblastoma Therapy: From Tumor to Its Microenvironment.International journal of molecular sciences · 2026Review
- Novel cilengitide derivatives suppress migration and invasion of temozolomide-resistant glioblastoma cells via MAPK/Akt pathway inhibition.Journal of neuro-oncology · 2026Article
- TEAD4-driven GPX8 promotes temozolomide resistance in glioma by facilitating CTHRC1 expression to suppress mitochondrial oxidative stress.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Targeting metabolic mechanisms to overcome temozolomide resistance in glioblastoma.Discover oncology · 2026Review
- Cardiac Glycosides: From Natural Defense Molecules to Emerging Therapeutic Agents.Biomolecules · 2025Review
- Silencing LINC01547 induces hepatocellular carcinoma cell apoptosis and metastasis inhibition via the ADAR1/FAK and miR-146b-5p/RAC1 axes.Apoptosis : an international journal on programmed cell death · 2025Article
- Review
- Mitochondrial Dysfunction: Effects and Therapeutic Implications in Cerebral Gliomas.Medicina (Kaunas, Lithuania) · 2024Review
- Bufotalin Induces Oxidative Stress-Mediated Apoptosis by Blocking the ITGB4/FAK/ERK Pathway in Glioblastoma.Antioxidants (Basel, Switzerland) · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiforme (GBM) is the most prevalent and lethal primary intracranial neoplasm in the adult population, with treatments of limited efficacy. Recently, bufotalin has been shown to have anti-cancer activity in a variety of cancers. This investigation aims to investigate the effect of bufotalin on GBM and elucidate its potential underlying mechanism. Our results show that bufotalin not only inhibits the proliferation and epithelial-mesenchymal transition (EMT) but also triggers apoptosis in GBM cells. The result of RNA-seq indicated that bufotalin could induce mitochondrial dysfunction. Moreover, our observations indicate that bufotalin induces an excessive accumulation of intracellular reactive oxygen species (ROS) in GBM cells, leading to mitochondrial dysfunction and the dephosphorylation of AKT. Moreover, bufotalin improved TMZ sensitivity of GBM cells
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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.