Liquiritin as a Tumor Suppressor Prevents the Development of Breast Cancer via the Epidermal Growth Factor Receptor/Mitogen-Activated Protein Kinase 8 Signaling Pathway

Abstract

Liquiritin, a key component extracted from Glycyrrhiza radix, exhibits a variety of physiological effects. This study investigates the role of liquiritin in the progression of breast cancer. This investigation conducted experiments using two breast cancer cell lines treated with varying concentrations of liquiritin, further validating our findings in vivo. Bioinformatics analysis was used to identify the pathways potentially regulated by liquiritin in breast cancer. The results indicated that the epidermal growth factor receptor (EGFR) and mitogen-activated protein kinase 8 (MAPK8) are potential downstream factors regulated by liquiritin in breast cancer. Our findings demonstrated that liquiritin significantly suppressed cell proliferation and induced cell cycle arrest in a dose-dependent manner. In addition, liquiritin triggered apoptosis by inhibiting the phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B signaling pathway. Liquiritin also reduced mitochondrial membrane potential, leading to mitochondrial dysfunction and promoting excessive reactive oxygen species (ROS) production by suppressing the EGFR/MAPK8 signaling pathway. Furthermore, liquiritin treatment resulted in a notable decrease in tumor size in breast cancer models through inhibiting cell proliferation and promoting apoptosis. In conclusion, liquiritin serves as an effective tumor suppressor, suppressing the proliferation and cell cycle progression of breast cancer cells, while inducing apoptosis by regulating mitochondrial function and ROS generation via the EGFR/MAPK8 signaling pathway.