The Effect of GADD45a on Furazolidone‐Induced S‐Phase Cell‐Cycle Arrest in Human Hepatoma G2 Cells |
| |
| Authors: | Yu Sun Shusheng Tang Xilong Xiao |
| |
| Affiliation: | 1. Department of Veterinary Public Health, China 2. Animal 3. Disease 4. Control Center, Beijing, People's Republic of China;5. Department of Pharmacology and Toxicology, College of Veterinary Medicine, China Agricultural University, Beijing, People's Republic of China |
| |
| Abstract: | In this study, overexpression of GADD45a induced by furazolidone in HepG2 cells could arouse S‐phase cell cycle arrest, suppress cell proliferation, and increase the activities of cyclin D1, cyclin D3, and cyclin‐dependent kinase 6 (CDK6). To the opposite, GADD45a knockdown cells by RNAi could reduce furazolidone‐induced S‐phase cell cycle arrest, increase the cell viability, decrease the activities of cyclin D1, cyclin D3, and CDK6; however, cyclin‐dependent kinase 4 (CDK4) showed no change. Moreover, data from our current studies show that cyclin D1, cyclin D3, and CDK6 are target genes functioning at the downstream of the GADD45a pathway induced by furazolidone. These results demonstrate that the GADD45a pathway is partially responsible for the furazolidone‐induced S‐phase cell cycle arrest. GADD45a influences furazolidone‐induced S‐phase cell cycle arrest in human hepatoma G2 cells via cyclin D1, cyclin D3, and CDK6, but not CDK4. |
| |
| Keywords: | GADD45a RNAi S‐phase cell cycle arrest Furazolidone cell viability human hepatoma G2 cells |
|
|
