Molecular Mechanism Discovery of Acacetin Against Cancers: Insights from Network Pharmacology and Molecular Docking

TL;DR

This paper explores how acacetin, a natural compound, fights cancer by combining computational and experimental methods to identify key molecular targets.

Contribution

The paper introduces a novel integrative framework combining network pharmacology and molecular docking with experimental validation.

Findings

Acacetin targets EGFR, STAT3, and AKT/PKB in cancer cells.

Network pharmacology and molecular docking reveal multi-target mechanisms of acacetin.

Experimental validation supports computational predictions of acacetin's anticancer effects.

Abstract

Acacetin, a naturally occurring flavonoid, has attracted increasing attention due to its broad anticancer potential. In vitro and in vivo studies using diverse tumor models have demonstrated that acacetin modulates oncogenic signaling, suppresses angiogenesis, and induces apoptosis and other regulated cell death pathways. With the rising demand for multi-target therapeutics, network pharmacology and molecular docking have emerged as powerful tools to unravel the complex molecular mechanisms of phytochemicals. Unlike previous reviews that have mainly focused on single pathways or limited cancer contexts, this review emphasizes novelty by integrating network pharmacology with molecular docking and explicitly linking these computational predictions to experimental validation, thereby identifying epidermal growth factor receptor (EGFR), signal transducer and activator of transcription 3 (STAT3), and the serine/threonine kinase AKT (also known as protein kinase B (PKB) as central experimentally supported targets. This integrative framework maps acacetin’s multi-target anticancer mechanisms and clarifies its translational opportunities for future therapeutic development.

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