Taraxasterol stimulates apoptosis of BCa cells via restraining PI3K/AKT and epidermal growth factor receptor (EGFR)

Abstract

Breast cancer (BCa) is a prevalent form of tumor, necessitating the development of more effective therapeutic drugs to improve patient prognosis. Taraxasterol (TAX), derived from the dandelion plant, has demonstrated significant physiological and pharmacological activity, but its role in BCa and underlying mechanism remains unexplored. In this study, we investigate the effects of TAX on the growth, motility and apoptosis of BCa cells in vitro to determine its mechanistic actions. Our results demonstrate that TAX significantly reduces both the proliferation and motility of BCa cells and induces apoptosis in BCa cells, as confirmed through flow cytometry (FCM). This apoptotic effect was further supported by JC-1 staining, which showed alterations in mitochondrial membrane potential in BCa cells after TAX treatment. Mechanistically, TAX suppresses the phosphatidylinositide 3-kinases/protein kinase B (PI3K/AKT) and EGFR pathways and impedes BCa progression. Collectively, TAX stimulates BCa cell apoptosis by inhibiting the PI3K/AKT and EGFR pathways.