ArticleAmerican journal of translational research2026
Brazilin induces apoptosis and autophagy in human glioblastoma cells via the PI3K/AKT/mTOR signaling pathway.
Article in American journal of translational research, 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesBrazilin (BZ), an active isoflavonoid from Chinese herbs, exhibits antitumor properties. This study investigated its antitumor efficacy and molecular mechanisms in human glioblastoma (GBM) cells.
methodsGBM cell proliferation and viability were assessed using xCELLigence RTCA eSight™, cell counting kit-8, 5-ethynyl-2'-deoxyuridine, live/dead staining, and colony formation assays. Migration and invasion were evaluated by Transwell, three-dimensional invasion, and wound healing assays. Apoptosis was analyzed by flow cytometry, and target protein expression by western blot. A xenograft model was established by subcutaneous injection of P3 cells into nude mice, followed by BZ treatment at different concentrations.
resultsBZ significantly inhibited GBM cell proliferation and viability in time- and dose-dependent manners. It also suppressed cell invasion and migration dose-dependently. Apoptosis rates in U251, P3, and LN229 cells increased significantly after BZ treatment. Accordingly, BZ upregulated the apoptosis-related proteins B-cell lymphoma 2 (BCL-2)-associated X protein and cleaved poly (ADP-ribose) polymerase-1, as well as the autophagy-related protein LC3B, while downregulating BCL-2 and sequestosome 1. Phosphorylated phosphoinositide 3-kinase (PI3K), protein kinase B (AKT), and mammalian target of rapamycin (mTOR) levels were reduced in BZ-treated U251 and LN229 cells. Finally, BZ inhibited the growth of orthotopic xenografts from luciferase-expressing P3 cells in mice.
conclusionsBZ induces apoptosis and autophagy in GBM cells via the PI3K/AKT/mTOR signaling pathway, suggesting its potential as a novel therapeutic agent for GBM patients.
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.