2016年11月
BUBR1 Insufficiency in Mice Increases their Sensitivity to Oxidative Stress
IN VIVO
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- 巻
- 30
- 号
- 6
- 開始ページ
- 769
- 終了ページ
- 776
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.21873/invivo.10993
- 出版者・発行元
- INT INST ANTICANCER RESEARCH
Background/Aim: Budding uninhibited by benzimidazole-related 1 (BUBR1) plays an important role in the spindle assembly checkpoint to prevent chromosome missegregation and aneuploidy during mitosis. We previously generated mutant mice that express BUBR1 at only 20% of the normal level (BubR1(L/L) mice). Here, we examined the effect of low BUBR1 expression on oxidative stress-induced carcinogenesis in mice. Materials and Methods: We orally administered either a potassium bromate (KBrO3) solution (2 g/l) or tap water to BubR1(L/L) and wild-type (BubR1(+/+)) mice for 16 weeks and examined the subsequent incidence of tumours. Results: KBrO3-treated BubR1(L/L) mice showed significantly higher mortality than the KBrO3-treated BubR1(+/+) and control tap water-treated mice (p=0.0082). Histopathological and immunohistochemical analyses revealed that the spleens of surviving BubR1(L/L) mice were occupied by non-B-, non-T-cells with high proliferative potential. Conclusion: Our results indicate that low BUBR1 expression increases oxidative stress-induced mortality in mice, possibly caused by splenic neoplasms.
- リンク情報
- ID情報
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- DOI : 10.21873/invivo.10993
- ISSN : 0258-851X
- eISSN : 1791-7549
- PubMed ID : 27815460
- Web of Science ID : WOS:000392926200007