WEKO3
アイテム
A Loss of Function Screening for Radiation Susceptibility Genes
https://repo.qst.go.jp/records/69031
https://repo.qst.go.jp/records/69031cd8ed7d0-7ae5-46f6-9ab9-16b3208115bc
| Item type | 会議発表用資料 / Presentation(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2007-07-18 | |||||
| タイトル | ||||||
| タイトル | A Loss of Function Screening for Radiation Susceptibility Genes | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_c94f | |||||
| 資源タイプ | conference object | |||||
| アクセス権 | ||||||
| アクセス権 | metadata only access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
| 著者 |
Sudou, Hitomi
× Sudou, Hitomi× Tsuji, Atsushi× Sugyou, Aya× Sogawa, Chizuru× Saga, Tsuneo× Harada, Yoshinobu× 須藤 仁美× 辻 厚至× 須尭 綾× 曽川 千鶴× 佐賀 恒夫× 原田 良信 |
|||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Carcinogenesis is thought to be a multistep process that occurs through the accumulation of mutations in multiple genes required for the maintenance of normal growth control. Genomic instability is considered the earliest cellular event in the process of carcinogenesis. Although genomic instability is induced by ionizing radiation, the molecular mechanisms underlying this process are poorly understood. Cell cycle checkpoints play a key role in cell survival following DNA damage. The failure of DNA repair and cell cycle regulation in response to DNA damage are thought to be important factors in the early stages of genomic instability. Several known genes are reportedly associated not only with DNA damage repair and cell cycle regulation but also with radiation susceptibility. Thus, the identification of novel radiation susceptibility genes will likely help elucidate the molecular mechanisms underlying DNA damage–induced genomic instability. By the large-scale expression profiling of 15 human cell lines and three mouse strains having varying degrees of susceptibility to ionizing radiation, we identified 200 genes correlated with radiation susceptibility. We constructed the shRNA library of these 200 genes and screened this library using a 96-well format and measuring the cell survivals, as determined by a sulforhodamine B–based cell proliferation assay, after X-irradiation. We identified 12 genes involved in cellular proliferation after irradiation. Three genes, ATM, ATR and CDKN1A, were known to be radiation susceptibility genes and other nine genes have not been reported to be associated with radiation susceptibility. Eight of the 12 genes were reported to directly or potentially regulate cell cycle, and the remaining four genes have not been reported biological functions. We then performed cell cycle analysis of cells transfected with shRNA vectors against thee four genes following X-irradiation, and found that knockdown cells of one gene did not accumulate at G2/M phase. This result suggests that one gene is associated with G2/M checkpoint after DNA damage. Further study of these 12 genes would help elucidate the molecular mechanism for genomic instability and carcinogenesis, and develop novel drugs for effective tumor radiotherapy and early diagnosis. |
|||||
| 会議概要（会議名, 開催地, 会期, 主催者等） | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | １３ｔｈ International Congress of Radiation Reserch | |||||
| 発表年月日 | ||||||
| 日付 | 2007-07-12 | |||||
| 日付タイプ | Issued | |||||
