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

Abstract

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.

Keywords

• CoQ0
• TNBC
• Apoptosis
• Autophagy
• ROS