calyculin-a has been researched along with Carcinoma--Hepatocellular* in 2 studies
2 other study(ies) available for calyculin-a and Carcinoma--Hepatocellular
| Article | Year |
|---|---|
Involvement of K(+)-Cl(-)-cotransport in the apoptosis induced by N-ethylmaleimide in HepG2 human hepatoblastoma cells.
The role of K(+)-Cl(-)-cotransport in apoptosis in human cancer cells was investigated. N-Ethylmaleimide, a K(+)-Cl(-)-cotransport activator, induced apoptosis in a dose-dependent manner in HepG2 human hepatoblastoma cells. N-Ethylmaleimide induced Cl(-)-dependent K(+) efflux, indicating that K(+)-Cl(-)-cotransport is functionally present in HepG2 cells. Calyculin-A and genistein, inhibitors of K(+)-Cl(-)-cotransport, significantly prevented both K(+)-Cl(-)-cotransport activation and apoptosis induced by N-ethylmaleimide. These results demonstrate, for the first time, a novel role for K(+)-Cl(-)-cotransport in apoptosis in human hepatoma cells. These results further suggest that K(+)-Cl(-)-cotransport may be a valuable target for therapeutic interventions for human hepatoma. Topics: Apoptosis; Carcinoma, Hepatocellular; Carrier Proteins; Chlorides; Ethylmaleimide; Flow Cytometry; Genistein; Humans; Ion Transport; K Cl- Cotransporters; Marine Toxins; Oxazoles; Potassium; Symporters; Tumor Cells, Cultured | 2001 |
Role of reactive oxygen species generated by NADPH oxidase in the mechanism of activation of K(+)-Cl(-)-cotransport by N-ethylmaleimide in HepG2 human hepatoma cells.
K(+)-Cl(-)-cotransport (KCC) is ubiquitously present in all cells, and plays an essential role in ion and volume regulation. In this study we investigated the role of reactive oxygen species (ROS) in regulation of KCC in HepG2 human hepatoblastoma cells. N-ethylmaleimide (NEM), a KCC activator, induced Cl(-)-dependent K+ efflux, which was markedly prevented by KCC inhibitors (calyculin-A, genistein and BaCl2), indicating that KCC is activated by NEM in the HepG2 cells. Treatment with NEM also induced a sustained increase in the level of intracellular ROS assessed by 2',7'-dichlorofluorescein fluorescence. Antioxidants, N-acetyl cysteine or N,N'-diphenyl-p-phenylenediamine significantly inhibited both ROS generation and KCC activation induced by NEM. The NEM-induced ROS production was significantly suppressed by inhibitors of NADPH oxidase (diphenylene iodonium, apocynin and neopterine). These inhibitors also significantly inhibited the NEM-induced KCC activation. Taken together, these results suggest that ROS generated by NADPH oxidase may mediate the NEM-induced activation of KCC in human hepatoma cells. Topics: Carcinoma, Hepatocellular; Chlorides; Enzyme Inhibitors; Ethylmaleimide; Genistein; Humans; K Cl- Cotransporters; Liver Neoplasms; Marine Toxins; NADPH Oxidases; Oxazoles; Potassium; Reactive Oxygen Species; Symporters; Tumor Cells, Cultured | 2001 |