Pyrroloquinoline quinone induces chondrosarcoma cell apoptosis by increasing intracellular reactive oxygen species

Pyrroloquinoline quinone (PQQ) has been reported to contribute to cancer cell apoptosis and death; however, little is known of its underlying mechanisms. The present study was designed to investigate the role of PQQ in chondrosarcoma cell apoptosis and the underlying mechanism. A cell cytotoxicity assay was used to detect cell death; flow cytometry analysis was also performed to determine cell apoptosis and intracellular reactive oxygen species (ROS). Biochemical methods were employed to detect the activity and the expression of superoxide dismutase (SOD)1, SOD2 and glutathione. The present study also examined the effect on tumorigenesis in vivo. The results demonstrated that the apoptosis of SW1353 cells induced by PQQ increased in a concentration‑ and time‑dependent manner, which may be attributable to the accumulation of intracellular ROS. In the in vivo experiments, PQQ inhibited proliferation and promoted apoptosis, increased ROS levels and caused DNA damage in transplanted cells. Taken together, the findings of the present study confirmed that PQQ induced apoptosis in human chondrosarcoma SW1353 cells and transplanted cells, by increasing intracellular ROS and reducing the ability of scavenging oxygen free radicals.