title: [Molecular mechanism of cell death by radiation].
abstract: p53 protein, a tumor suppressor protein, is accumulated and activated by ionizing radiation. It activates various downstream genes whose functions are involved in cell cycle arrest, apoptosis, and DNA repair. Although it was thought generally that G1 arrest by p53 activation after ionizing radiation was a transient phenomenon to facilitate DNA repair, we found that it is irreversible and permanent in both normal human cells and tumor cells. Because cells arrested irreversibly express various phenotypes, such as cell enlargement and expression of senescence associated-beta-gal, this is related to cellular senescence, but not to apoptosis. Therefore, we termed this phenomenon senescence-like growth arrest (SLGA). These results indicate that SLGA is the main form of cell death caused by ionizing radiation. SLGA can be utilized as an index of cancer therapy, because it is induced not only by radiation but also by anticancer drugs and is easy to examine by vital staining, thereby making the induction of SA-beta-gal an index.
authors.affiliation: Division of Radiation Biology, Graduate School of Biomedical Sciences, Nagasaki University.
authors.forename: Masami
authors.initials: M
authors.lastname: Watanabe
authors.forename: Keiji
authors.initials: K
authors.lastname: Suzuki
authors.forename: Seiji
authors.initials: S
authors.lastname: Kodama
mesh_terms: D017209:Apoptosis / Q000235:genetics / Q000528:radiation effects; D002453:Cell Cycle / Q000528:radiation effects; D016923:Cell Death / Q000235:genetics / Q000528:radiation effects*; D016922:Cellular Senescence / Q000502:physiology / Q000528:radiation effects*; D006801:Humans; D009369:Neoplasms / Q000235:genetics / Q000473:pathology* / Q000532:radiotherapy; D016159:Tumor Suppressor Protein p53 / Q000502:physiology; D001616:beta-Galactosidase / Q000378:metabolism
chemical_list: D016159:Tumor Suppressor Protein p53; D001616:beta-Galactosidase