Pyrroloquinoline quinone (PQQ) has been reported as a promising agent that might contribute to
tumor cell apoptosis and death, yet little is known on its mechanisms. In current study, the effect of PQQ on cell proliferation and mitochondrial-dependent apoptosis were examined in 3 solid tumor cell lines (A549, Neuro-2A and HCC-LM3). PQQ treatment at low to medium dosage exhibited potent anti-
tumor activity on A549 and Neuro-2A cells, while had comparably minimal impact on the viabilities of 2 human normal cell lines (HRPTEpiC and HUVEC). The apoptosis of the 3 tumor cell lines induced by PQQ were increased in a concentration-dependent manner, which might be attributed to the accumulation of intracellular
reactive oxygen species (ROS), decline in
ATP levels and dissipation of mitochondrial membrane potential (
MMP), in conjunction with down-regulation of Bcl-2
protein expression, up-regulation of activated
caspase-3, and disturbed phosphorylated MAPK
protein levels. PQQ induced
tumor cells apoptosis was significantly alleviated by pan-
caspase inhibitor
Z-VAD-FMK. The present work highlights the potential capability of PQQ as an anti-
tumor agent with low toxicity towards normal cells through activating mitochondrial-dependent apoptosis pathways, and warrants its development for
cancer therapy.