Exploring Molecular Targets and Mechanisms of Apigenin in the Treatment of Papillary Thyroid Carcinoma Based on Network Pharmacology and Molecular Docking Analysis

Abstract

To explore potential therapeutic targets and underlying mechanisms of apigenin (API) for papillary thyroid carcinoma (PTC) treatment. Methods: In the present study, network pharmacological analysis combined with molecular docking was used to identify API-related therapeutic targets for PTC treatment. Firstly, potential API-interacting and PTC-related targets were obtained from online databases. Furthermore, we constructed drug-target-disease interaction networks followed by functional enrichment analysis, expression patterns and prognostic values of predicted core targets by using bioinformatic tools. Moreover, we performed molecular docking to validate binding activity of API to core pharmacological targets. Results: A total of 110 API-related therapeutic targets were found to be engaged in the treatment of PTC. Moreover, TP53, HSP90AA1, AKT1, EGFR, SRC, VEGFA, ACTB, JUN and ESR1 were identified as core pharmacological targets of API for treating PTC. The enrichment analysis suggested that API played a comprehensive role in regulating the apoptotic process, modulating cell proliferation, and that multiple pathways were involved in API-related PTC treatment. Further results indicated that the PI3k-Akt/p53 signaling pathway was the key signaling pathway. Moreover, JUN was found mostly correlated with survival and molecular docking results demonstrating strong affinities between API and these core targets. Conclusion: Our findings systematically demonstrated API-associated pharmacological targets and mechanisms for treating PTC and demonstrated that API could function against PTC by inducing apoptosis, cell death and immunological reactions. Our research gives valuable insights and a theoretical basis for API-related PTC treatment.