Abstract
Aim of the study: To analyze the chemical components of BSCO, evaluate its effects on lung cancer through vivo and vitro experiments, reveal its underlying mechanism in a rat model of LC. Methods: Ultra-high performance liquid chromatography with quadrupole time-of-flight mass spectrometry was used to identify components of BSCO. A Lewis lung cancer model was established in mice to evaluate the effects of BSCO by observing tissue morphology, whole animal imaging, and determination of serum biochemical indicators. The effects of BSCO on Lewis cancer cells in vitro were assessed using a CCK-8 cell proliferation assay. Network pharmacology and transcriptomics analysis was used to predict their targets and signaling pathways associated with lung cancer. The mRNA expressions of target genes were measured by RT-qPCR. Results: Twenty major chemical components of BSCO were identified. BSCO effectively inhibited tumor growth in the Lewis lung cancer mouse model and normalized serum markers of cancer to varying degrees. The IC50 of BSCO on Lewis cell proliferation was 173 mg/mL. Low- and high-dose BSCO-containing drug serum inhibited proliferation of Lewis cells after 24 and 48 h incubation. Integrated network pharmacology and transcriptomic analyses suggest that BSCO may exert anti-tumor effects through the PI3K-Akt signaling pathway, with TP53, IL6, CDKN1A, and KIT identified as potential key targets within this pathway. The reliability of the transcriptomic results was confirmed by verifying some lung cancer-related genes through RT-qPCR. BSCO was evaluated against model control and cyclophosphamide. A key follow-up step will be to perform protein-level validation, which confirms the observed transcriptomic signals. Conclusion: BSCO significantly inhibited lung cancer growth in vitro and in vivo. Network pharmacology and transcriptomics suggested that its anti-cancer effects might involve the PI3K-Akt signaling pathway, TP53, IL6, CDKN1A, and KIT may be its key targets.