Thymoquinone regulates osteosarcoma cell proliferation through the P53 signaling pathway: A network pharmacology and molecular docking based health technology study

Background Osteosarcoma (OS) has long presented a formidable challenge to human health and well-being. While traditional treatments, such as clinical chemotherapy and surgical intervention, have shown efficacy, they are frequently accompanied by adverse effects and often lead to a poor prognosis. Objective Thymoquinone (TQ) is recognized for its antitumor properties; however, the specific molecular mechanisms underlying its effects against OS remain inadequately understood. Emerging evidence suggests a strong correlation between p53 gene deletion and the onset and progression of various human cancers. This study aimed to elucidate the pharmacological targets and anti-OS mechanisms of TQ using systems bioinformatics approaches, including network pharmacology and molecular docking simulations. Methods A comprehensive screening process identified 23 potential targets associated with the anti-OS effects of TQ. Subsequent bioinformatics analysis identified 8 core targets involved in TQ's anti-OS activity. Enrichment analysis indicated that these core targets modulate a range of biological processes and may influence multiple molecular pathways. Results Preliminary in vitro data indicated that TQ effectively reduces OS cell proliferation, induces apoptosis, and downregulates the expression of P53 and HMOX1 proteins. Conclusion Our findings elucidate the molecular mechanisms underlying TQ's effectiveness against OS, highlighting potential apoptosis-related therapeutic targets, such as P53 and CYCLIN D1, for the treatment of OS with TQ.