Life sciences · Journal article
Discovery Medicine · September 23, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Background: Although psoralen is known for its antitumor and chemosensitizing effects across multiple malignancies, its function and molecular basis in bladder cancer (BC) remain insufficiently understood. Thus, this study examined its anti-cancer actions in BC and identified its potential target.Methods: Human BC cell lines (5637, T24, UM-UC-3, and J82) and a normal bladder epithelial cell line (SV-HUC-1) were exposed to graded psoralen doses. Cell viability and proliferation were evaluated using Cell Counting Kit-8 (CCK-8) and colony formation assays, while apoptosis was analyzed via flow cytometry. Potential psoralen-related targets and BC-associated genes were identified using public databases and intersected via Venny analysis. The expression of aurora kinase A (AURKA) was analyzed using bioinformatics platforms and validated using quantitative reverse transcription polymerase chain reaction and Western blotting. Functional experiments involving AURKA overexpression were conducted to determine its role in mediating psoralen responses. Expression levels of apoptosis- and proliferation-related proteins, including proliferating cell nuclear antigen (PCNA), B-cell lymphoma-2 (Bcl-2), cleaved caspase-3, and Bcl-2-associated X protein (Bax), were also examined.Results: Psoralen dramatically decreased BC cell viability and colony-forming ability while markedly promoting apoptosis (p < 0.05). Psoralen treatment upregulated cleaved caspase-3 and Bax, and downregulated PCNA and Bcl-2 (p < 0.01). Through bioinformatics analysis, AURKA was found to be upregulated in BC tissues and cell lines (p < 0.05). Psoralen reduced AURKA expression, and overexpression of AURKA partially attenuated psoralen-induced proliferation inhibition and apoptosis (p < 0.05).Conclusion: In vitro, psoralen suppresses BC cell proliferation and promotes apoptosis, and AURKA may be involved in these effects. These results point to psoralen as a promising natural compound for further investigation in BC therapy.