Control of radiation-induced G1 arrest by cell-substratum interactions.
Ionizing radiation has been reported to cause an irreversible, senescence-like G1 arrest in human fibroblasts, which is accompanied by elevated p21CIP1 amounts. In further support of a senescence-like arrest, we show that expression of p53 and cyclin D1 is elevated in gamma-irradiated, arrested fibroblasts. However, we also demonstrate that the arrest is reversible if the irradiated cells are trypsinized and replated, which may implicate cellular-extracellular matrix interactions in cell cycle control after irradiation.
Gadbois
D M
DM
Life Sciences Division, Los Alamos National Laboratory, New Mexico 87545, USA.
Bradbury
E M
EM
Lehnert
B E
BE
D002448:Cell Adhesion; D018929:Cell Culture Techniques / Q000379:methods; D002455:Cell Division / Q000528:radiation effects; D002478:Cells, Cultured; D019938:Cyclin D1; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins / Q000096:biosynthesis / Q000235:genetics; D005109:Extracellular Matrix / Q000502:physiology*; D005347:Fibroblasts / Q000166:cytology / Q000528:radiation effects*; D016193:G1 Phase / Q000528:radiation effects*; D005720:Gamma Rays; D016158:Genes, p53; D006801:Humans; D015513:Oncogene Proteins / Q000096:biosynthesis / Q000235:genetics; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis
C493956:CDKN1A protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D015513:Oncogene Proteins; D016159:Tumor Suppressor Protein p53; D019938:Cyclin D1