Revealing the Anticancer Mechanism of Cephaibol A, a Peptaibol Isolated from <i>Acremonium tubakii</i> BMC-58, Triggering Apoptosis <i>via</i> the Mitochondrial Pathway in Human Breast Cancer Cells

Cephaibol A was isolated from a freshwater fungus Acremonium tubakii BMC-58 extract which composed of 16 amino acids and featuring multiple α-aminoisobutyric acid. We investigated the cytotoxicity of cephaibol A on MDA-MB-231 cells to elucidate its potential antitumor activity and mechanism. The study found that cephaibol A concentration-dependently blocked the cell cycle in S phase and inhibited cell proliferation. Meanwhile, cephaibol A could reduce the migration and invasion abilities of MDA-MB-231 cells. Further studies proved that cephaibol A caused mitochondrial dysfunction and increased reactive oxygen species (ROS) accumulation. Mitochondrial membrane potential (ΔΨm) assay suggested that cephaibol A induced apoptosis by affecting Bcl-2, Bax and cytochrome c levels, thus decreasing ΔΨm and activating the caspase cascade reaction. Moreover, cephaibol A significantly inhibited tumor growth and improved survival rates in the MDA-MB-231 cell mice model. These findings established cephaibol A as a potential antitumor agent that inhibited tumor cell proliferation in vitro and in vivo by affecting mitochondrial dysfunction and inducing apoptosis in MDA-MB-231 cells through structural damage.