β-eudesmol inhibits cell proliferation and induces ferroptosis via regulating MAPK signaling pathway in breast cancer

The aim of this study was to explore the influences and underlying mechanisms of β-eudesmol on breast Cancer (BC). Different concentrations of β-eudesmol (0, 10, 20, and 40 μM) were taken to treat BC cells. Cell Counting Kit-8, colony formation assay, and flow cytometry were performed to evaluate the influences of β-eudesmol on cell viability, proliferation, and Apoptosis. To assess the influences of β-eudesmol on cell Ferroptosis, the change of ROS, SOD, MDA, and intracellular iron and Fe²⁺ were determined. The protein changes of Apoptosis, Ferroptosis, and MAPK pathway (Bcl-2, Bax, cleaved Caspase-3, SLC7A11, GPX4, SLC40A1, Transferrin, MEK1, and ERK1/2) were checked utilizing Western blot. In a concentration-dependent manner, β-eudesmol restrained cell viability and proliferation. β-eudesmol promoted cell Apoptosis, as evidenced by the decline level of Bcl-2 and the raised level of Bax and cleaved Caspase-3. β-eudesmol enhanced the level of ROS, MDA, iron, Fe²⁺, and Transferrin, and lessened SOD activity and the protein expression of SLC7A11, GPX4, SLC40A1, MEK1, and ERK1/2. Moreover, Ferroptosis inhibitor Fer-1 and MEK1 overexpression both reversed the changes on cell proliferation, Apoptosis, and Ferroptosis induced by β-eudesmol. β-eudesmol inhibited cell proliferation and promoted cell Apoptosis and Ferroptosis via regulating MAPK pathway in BC.