@article{oai:repo.qst.go.jp:00047001,
 author = {二宮, 康晴 and 崔, 星 and 安田, 武嗣 and 王, 冰 and 于, 冬 and 関根, 絵美子 and 根井, 充 and 二宮 康晴 and 崔 星 and 安田 武嗣 and 王 冰 and 于 冬 and 関根 絵美子 and 根井 充},
 issue = {10},
 journal = {BMB Reports},
 month = {Feb},
 note = {Arsenite is a potent anticancer agent for many human cancers. In this study, we investigate whether arsenite-induced DNA damage leads to p53-dependent premature senescence using human glioblastoma cells with p53-wild type (U87MG-neo) and p53 deficient (U87MG-E6). Arsenite dose-dependently reduced cell growth, and low concentration of arsenite significantly induced γH2AX foci formation both in U87MG-neo and U87MG-E6 cells. However, senescence was induced by arsenite with senescence-associated β-galactosidase staining and dimethyl- and trimethyl-lysine 9 of histone H3 (H3DMK9 and H3TMK9) foci formation accompanied by p21 accumulation only in U87MG-neo, suggesting that arsenite induces premature senescence as a result of DNA damage with heterochromatin formation through p53/p21 dependent pathway. Consistently, p21 and p53 siRNA decreased H3TMK9 foci formation in U87MG-neo treated with arsenite. Taken together, arsenite reduces cell growth p53-independently and induces premature senescence via p53/p21-dependent pathway following DNA damage. This finding explored new anti-tumor mechanisms induced by arsenite.},
 pages = {575--580},
 title = {Arsenite induces premature senescence via p53/p21 pathway as a result of DNA damage in human malignant glioblastoma cells},
 volume = {47},
 year = {2014}
}