A novel pyrazolone-based derivative induces apoptosis in human esophageal cells via reactive oxygen species (ROS) generation and caspase-dependent mitochondria-mediated pathway

- Cd-PMPP-SAL inhibited Eca-109 cells proliferation.
- Cd-PMPP-SAL-treated Eca-109 cells showed typical apoptotic features.
- Cd-PMPP-SAL promoted the production of ROS and loss of ΔΨm.
- Cd-PMPP-SAL induces apoptosis via caspase-dependent mitochondrial-mediated pathway.

Pyrazolone complexes have strong bio-activity but the anti-tumor mechanism of pyrazolone-based metal complexes is not fully understood. In this study, the inhibitory effect and possible mechanism of a novel pyrazolone-based derivative compound (Cd-PMPP-SAL) on human esophageal cancer cells were investigated. We found that Cd-PMPP-SAL inhibited the proliferation of Eca-109 cells in a dose-dependent manner and induced the apoptosis in the cells. Interestingly, Cd-PMPP-SAL promoted the production of ROS, loss of mitochondrial membrane potential, PARP cleavage and activation of caspase-3/9. These results suggest Cd-PMPP-SAL-induced apoptosis might be mediated by the increased production of ROS and caspase-dependent mitochondria-mediated pathway. These results suggest that Cd-PMPP-SAL is a potential candidate for the treatment of esophageal cancer.