Abstract
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
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.
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