ArticleScientific reports2026
Combining network pharmacology and experimental validation to study the action and mechanism of brusatol against lung adenocarcinoma.
Article in Scientific reports, 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brusatol is a natural product found in the plant Brucea javanica that is used to treat diseases such as amoebiasis and malaria. It also has significant anti-tumor effects. However, its role in lung cancer and the mechanism underlying its pharmacological effects remain unclear. In this study, we identified the core target of brusatol for lung adenocarcinoma (LUAD) therapy using network pharmacology and elucidated its therapeutic mechanism by conducting cell experiments. The therapeutic targets of brusatol were obtained from the PharmMapper database, the LUAD-related genes were obtained from the TCGA database, and the intersection targets of the two were taken as potential targets for treating LUAD with brusatol. Based on the results of the intersection, core target and signaling pathways were identified by protein-protein interaction (PPI), molecular docking, gene ontology (GO) function, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. Finally, cell experiments were performed to determine the antineoplastic effect of brusatol on LUAD. We identified 328 potential targets of brusatol for treating LUAD, and the PPI network analysis identified ALB, SRC, HSP90AA1, HRAS, CASP3, MAPK1, and ESR1 as key genes. Through molecular docking, MAPK1 was identified as the core target of brusatol in LUAD. GO analysis revealed that brusatol may exert anti-tumor effects through endopeptidase activity, protein tyrosine kinase activity, and amide binding. KEGG enrichment analysis suggested that brusatol may treat LUAD by regulating the RAS signaling pathway. Brusatol inhibited the proliferation and invasion of LUAD cells and caused apoptosis and G2/M phase arrest in these cells. Further analysis confirmed that brusatol plays a role in treating LUAD by targeting MAPK1 and regulating the Ras signaling pathway. To summarize, through a combination of network pharmacological analysis and cell experimental validation, we revealed the mechanism underlying the therapeutic effects of brusatol on LUAD. This study also provided a theoretical basis for using brusatol as a candidate drug for the targeted therapy of LUAD.
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.