サイトウ　タイイチ   SAITO Taiichi   齋藤　太一    所属   研究施設 研究施設    職種   非常勤講師
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	p16 Gene Transfer Induces Centrosome Amplification and Abnormal Nucleation Associated with Survivin Downregulation in Glioma Cells.
掲載誌名	正式名：Pathobiology : journal of immunopathology, molecular and cellular biology 略　 称：Pathobiology ISSNコード：1423-0291(Electronic)1015-2008(Linking)
掲載区分	国外
巻・号・頁	82(1),pp.1-8
著者・共著者	Takayasu Takeshi, Hama Seiji, Yamasaki Fumiyuki, Saito Taiichi, Watanabe Yosuke, Nosaka Ryo, Sugiyama Kazuhiko, Kurisu Kaoru
発行年月	2015/02
概要	OBJECTIVE:In human glioma cells, p16 gene transfer induced G1/S arrest, increased radiosensitivity and abnormal nucleation (especially bi- and multinucleation). Survivin suppression caused G2/M arrest, radiosensitization and an increase in aneuploidy accompaOBJECTIVE:nied by centrosome amplification. Abnormal nucleation and aneuploidy represent chromosome instability (CIN), and it is well known that centrosome amplification leads to CIN. However, little has been reported that suggests that transferring p16 causes centrosome overduplication during the G1/S phase.METHODS:The p16 gene was transferred into p16-null human glioma cell lines (U251MG and D54MG) using adenovirus with or without irradiation. Centrosome amplification was evaluated by immunofluorescence. We also investigated the DNA replication licensing factor CDT1, its inhibitor geminin and survivin expression as regulators of chromosomal segregation.RESULTS:p16 gene transfer with radiation initiated the greatest degree of centrosome overduplication. CDT1 showed low levels, geminin was unchanged and survivin decreased in Ax-hp16-infected cells with radiation. Those changes of factors affecting DNA licensing or chromosomal segregation might contribute to CIN.CONCLUSION:p16 transfer caused centrosome amplification even in G1/S phase-arrested cells. This suggests that p16 is involved in abnormal nucleation and radiosensitization in human glioma cells. © 2015 S. Karger AG, Basel.
DOI	10.1159/000368196
文献番号	25765578