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p16 Gene Transfer Induces Centrosome Amplification and Abnormal Nucleation Associated with Survivin Downregulation in Glioma Cells
Author(s) -
Takeshi Takayasu,
Seiji Hama,
Fumiyuki Yamasaki,
Taiichi Saito,
Yosuke Watanabe,
Ryo Nosaka,
Kazuhiko Sugiyama,
Kaoru Kurisu
Publication year - 2015
Publication title -
pathobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.941
H-Index - 53
eISSN - 1423-0291
pISSN - 1015-2008
DOI - 10.1159/000368196
Subject(s) - centrosome , survivin , microbiology and biotechnology , biology , cancer research , chromosome instability , mitosis , radiosensitivity , cell cycle , chemistry , cell culture , cell , chromosome , gene , genetics , medicine , radiation therapy
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 accompanied 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.

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