Control of cell cycle progression in human mesothelioma cells treated with gamma interferon
| Autor: | Jocelyne Fleury-Feith, I Monnet, F Levy, P Chretien, Y. Pilatte, Claire Vivo, Laurence Kheuang, M C Jaurand |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
Cyclin-Dependent Kinase Inhibitor p21
G2 Phase Mesothelioma Cancer Research Pleural Neoplasms Cyclin D Blotting Western Cyclin A Cyclin B Antineoplastic Agents Cell Cycle Proteins Transfection Interferon-gamma Cyclins Tumor Cells Cultured Genetics Humans Cyclin B1 Molecular Biology Cyclin Cyclin-dependent kinase 1 biology Cell growth Tumor Suppressor Proteins Cell cycle Flow Cytometry Cyclin-Dependent Kinases Recombinant Proteins Cell biology Enzyme Induction Cytogenetic Analysis biology.protein Electrophoresis Polyacrylamide Gel Tumor Suppressor Protein p53 Microtubule-Associated Proteins Protein Kinases Cell Division Cyclin-Dependent Kinase Inhibitor p27 DNA Damage Thymidine |
| Zdroj: | Oncogene. 20:1085-1093 |
| ISSN: | 1476-5594 0950-9232 |
| DOI: | 10.1038/sj.onc.1204199 |
| Popis: | Recombinant human interferon gamma (r-hu-IFNgamma) exerts both antitumoral activity in the early stages of human malignant mesothelioma and a cytostatic effect in human mesothelioma (HM) cell lines in vitro. The antiproliferative effect of interferons (IFNs) reported in a variety of cells has been attributed to several mechanisms. In order to progress in the understanding of HM cell growth modulation by r-hu-IFNgamma, modifications of cell cycle progression and expression of key cell cycle regulator proteins in response to r-hu-IFNgamma were examined. Nine HM cell lines were studied, including one resistant to the antiproliferative effect of r-hu-IFNgamma. Except in the resistant cell line r-hu-IFNgamma produced an arrest in the G1 and G2-M phases of the cell cycle, associated with a reduction in both cyclin A and cyclin dependent kinase inhibitors (CDKIs) expression. Moreover cyclin B1/cdc2 activity was decreased. The present study provides the first evidence of a G2-arrest in r-hu-IFNgamma-treated HM cell lines and indicates that HM cell lines, despite their tumorigenic origin still support cell cycle control. The cell cycle arrest induced by r-hu-IFNgamma seems to depend on cyclin regulation through p21(WAF1/CIP1)- and p27(Kip1)-independent mechanisms and is not directly related to the induced DNA damage. |
| Databáze: | OpenAIRE |
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