Arctigenin as a promising anticancer agent: a comprehensive review of molecular mechanisms across major carcinomas.

Despite the presence of numerous efficacious bioactive compounds, the development of effective cancer therapies remains necessary. Thus, the exploitation of the medicinal potential of bioactive compounds in cancer management has become an urgent demand. Arctigenin (AG), a natural lignin derived from Arctium lappa, not only suppresses the proliferation of diverse cancerous cells, including those in the liver, stomach, lungs, and colon, but also modulates various antitumor, intracellular, antioxidative, and anti-inflammatory activities. Arctigenin has also been shown to overcome tumor resistance via cell-cycle arrest, activation of apoptotic pathways, caspase activation, and proteasome regulation. It also downregulates numerous factors implicated in tumor migration and angiogenesis, including VEGF, matrix metalloproteinases, TGF-β, and N-cadherin. The restricted solubility of arctigenin in water indicates that modifying this compound through amino acid esterification may enhance its pharmacogenetic properties. The use of arctigenin or its derivatives may facilitate the development of novel chemotherapeutic strategies for future therapies. This review identifies common therapeutic targets and cancer-specific responses by comparing mechanistic insights across prostate, cervical, pharyngeal, and other carcinomas. Arctigenin is positioned as a viable option in anticancer research through a critical assessment of current limitations in preclinical and clinical research and by providing future perspectives on translational potential, drug development techniques, and combination therapies. Although there are publications that summarize the mechanism of action of arctigenin, none have explicitly elaborated on its anticancer mechanism across various carcinomas.