pyrazolone and Esophageal-Neoplasms

pyrazolone has been researched along with Esophageal-Neoplasms* in 1 studies

Other Studies

1 other study(ies) available for pyrazolone and Esophageal-Neoplasms

Article	Year
A novel pyrazolone-based derivative induces apoptosis in human esophageal cells via reactive oxygen species (ROS) generation and caspase-dependent mitochondria-mediated pathway. Chemico-biological interactions, 2015, Apr-25, Volume: 231 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. Topics: Antineoplastic Agents; Apoptosis; Cadmium; Caspases; Cell Line, Tumor; Esophageal Neoplasms; Esophagus; Humans; Mitochondria; Pyrazolones; Reactive Oxygen Species; Signal Transduction	2015

Article

Year

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

Chemico-biological interactions, 2015, Apr-25, Volume: 231

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.

Topics: Antineoplastic Agents; Apoptosis; Cadmium; Caspases; Cell Line, Tumor; Esophageal Neoplasms; Esophagus; Humans; Mitochondria; Pyrazolones; Reactive Oxygen Species; Signal Transduction

2015