Conclusions
This study identified the molecular targets and underlying mechanisms of FZSBD treatment against CC and may provide clues for future research on the treatment of CC with FZSBD.
Methods
Multiple network pharmacology approaches were used to predict the molecular targets and underlying mechanisms of FZSBD against CC. The expression of potential molecular targets was determined. The effects of FZSBD on cell viability, proliferation, migration, invasion, and the cell cycle of CC cells were investigated. The therapeutic efficacy, hematological, immunological, and inflammatory data in patients with CC were evaluated after treatment with the XELOX regimen with and without FZSBD.
Results
A total of 912 potential targets in FZSBD and 2765 DEGs in CC specimens were screened. Five hub genes (TP53, MYC, VEGFA, CCND1, and IL1B) closely associated with immune-related signaling pathways and the cell cycle process were identified. The five hub genes were of prognostic value in CC. The gene and protein expression of the five hub genes was significantly higher in CC tumor tissue samples than that of normal tissue samples. Furthermore, with increasing doses, FZSBD increasingly inhibited growth, migration, and invasion, and suppressed the cell cycle process of CC cells. Supplementing of FZSBD to the XELOX regimen enhanced immune modulation and alleviated inflammatory responses. Conclusions: This study identified the molecular targets and underlying mechanisms of FZSBD treatment against CC and may provide clues for future research on the treatment of CC with FZSBD.