fi -eudesmol inhibits cell proliferation and induces ferroptosis via regulating MAPK signaling pathway in breast cancer
TOXICON(2024)
摘要
The aim of this study was to explore the influences and underlying mechanisms of fi-eudesmol on breast cancer (BC). Different concentrations of fi-eudesmol (0, 10, 20, and 40 mu M) were taken to treat BC cells. Cell Counting Kit-8, colony formation assay, and flow cytometry were performed to evaluate the influences of fi-eudesmol on cell viability, proliferation, and apoptosis. To assess the influences of fi-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, fi-eudesmol restrained cell viability and proliferation. fi-eudesmol promoted cell apoptosis, as evidenced by the decline level of Bcl-2 and the raised level of Bax and cleaved caspase-3. fi-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 fi-eudesmol. fi-eudesmol inhibited cell proliferation and promoted cell apoptosis and ferroptosis via regulating MAPK pathway in BC.
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关键词
Breast cancer,fi-eudesmol,Cell proliferation,Ferroptosis,MAPK pathway
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