The anti-tumor activities of coenzyme Q0 through ROS-mediated autophagic cell death in human triple-negative breast cells

Coenzyme Q₀ (CoQ₀) obtained from Antrodia camphorata has therapeutic benefits in cancer treatment. Our previous findings in vivo and in vitro have shown that CoQ₀ affects triple-negative breast cancer cells (TNBCs) by blocking EMT and metastasis. The current study investigated the cancer-preventive activities of CoQ₀ on TNBC MDA-MB-468 and 231 cells by activating apoptotic and autophagic cell death. The CoQ₀ treatment reduced colony development and proliferation in TNBC cells. In addition, CoQ₀ triggered death activation by caspase-3 stimulation, PARP cleavage, and significantly affected Bax/Bcl-2 regulation. Autophagy was triggered by CoQ₀, as shown by LC3-II accumulation, p62/SQSTM1 expression, ATG5 expression, ATG4B inhibition, AVO formation, and impeded Beclin-1/Bcl-2 regulation. In addition, transmission electron microscopy data showed that CoQ₀ increased autophagosome formation. The antioxidant N-acetylcysteine substantially suppressed CoQ₀-mediated ROS generation and attenuated apoptotic- and autophagic-cell death by CoQ₀ in TNBC cells. CoQ₀ is a potential anticancer agent in treating human triple-negative breast cancers.