Deciphering the pharmacological mechanisms of salidroside in cervical cancer by combining network pharmacology, molecular docking, and in vitro studies

Cervical cancer is one of the major and serious risks to women. Salidroside, a natural compound, shows promise in treating cervical cancer. However, its specific molecular mechanisms remain unclear and require further investigation. This study aimed to elucidate the pharmacological activity of salidroside and its underlying molecular mechanisms in cervical cancer, employing network pharmacology, molecular docking, and experimental approaches. Genes associated with cervical cancer were gathered from The Cancer Genome Atlas Program (TCGA), Gene Expression Omnibus (GEO) databases, and network pharmacology. Furthermore, we integrated the drug targets with the disease targets pertinent to cervical cancer, subsequently conducting analyses utilizing the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) to explain the pharmacological pathways through which salidroside operates in the milieu of cervical cancer. Survival analysis was performed to screen the core therapeutic targets of salidroside. Salidroside constituents and hub genes binding affinity were assessed by molecular docking studies. In vitro experiments, including Cell Counting Kit-8 (CCK-8) assays, flow cytometry, and western blotting, were performed to further validate the computational findings. Study findings revealed that salidroside inhibited the cervical cancer cell progression, reduced viability, and induced apoptosis.Ten target genes related to salidroside's anti-cancer effects have been identified. Survival analysis revealed that MMP1 and MMP3 exhibited the highest binding capability among all the target genes. Molecular docking indicated that the salidroside's active entities showed a strong binding tendency with the MMP1 and MMP3 genes. Western blot analysis revealed that it significantly reduced the expression of MMP-1 and MMP-3. In Vitro studies suggested that suppressing MMP1 and MMP3 genes might be responsible for salidroside's anticancer effects.