福島県立医科大学学術成果リポジトリ = Fukushima Medical University Repository >
福島医学会 = The Fukushima Society of Medical Science >
Fukushima Journal of Medical Science >
Vol.61 (2015) >
このアイテムの引用には次の識別子を使用してください:
http://ir.fmu.ac.jp/dspace/handle/123456789/489
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タイトル: | Overexpression of both CLOCK and BMAL1 inhibits entry to S phase in human colon cancer cells |
著者: | Sakamoto, Wataru Takenoshita, Seiichi |
学内所属: | 器官制御外科学講座 |
誌名/書名: | Fukushima Journal of Medical Science |
巻: | 61 |
号: | 2 |
開始ページ: | 111 |
終了ページ: | 124 |
発行日: | 2015年 |
抄録: | Many physiological, biochemical and behavioral processes operate under the circadian rhythm, which is generated by an internal time-keeping mechanism commonly referred to as the biological clock, in almost all organisms from bacteria to mammals. The core circadian oscillator is composed of an autoregulatory transcription-translation feedback loop, in which CLOCK and BMAL1 are positive regulators. A cell has two mechanisms, "cell cycle" and "cell rhythm", the relationship between which remains controversial. Therefore, the aim of this study was to explore the effect of Clock and Bmal1 on cell cycle, especially on the G1 phase, using vectors with the tetracycline operator-repressor system. The present study revealed that simultaneous induction of Bmal1 and Clock had an influential effect on the cell cycle in SW480/T-REx/Clock/Bmal1 cells, in which both Clock and Bmal1 could be induced by tetracycline. The observation that induction of both Clock and Bmal1 inhibited cell growth and the significant increase of the G1 phase proportion of in SW480/T-REx/Clock/Bmal1 cells indicated that entry from the G1 to S phase was inhibited by the induction of Clock and Bmal1. Furthermore, overexpression of Clock and Bmal1 prevented the cells from entering into the G2/M phase induced by Paclitaxel, and made the cells more resistant to the agent. In conclusion, we found that overexpression of both Clock and Bmal1 suppressed cell growth. In addition, the present study raised the possibility that Clock and Bmal1 may in part play a role in preventing the cells from entering G1 to S phase of cell cycle via suppression of CyclinD1 expression, and thus acquiring resistance to Paclitaxel. |
出版者: | The Fukushima Society of Medical Science |
出版者(異表記): | 福島医学会 |
本文の言語: | eng |
このページのURI: | http://ir.fmu.ac.jp/dspace/handle/123456789/489 |
本文URL: | http://ir.fmu.ac.jp/dspace/bitstream/123456789/489/1/FksmJMedSci_61_p111.pdf |
ISSN: | 0016-2590 2185-4610 |
DOI: | 10.5387/fms.2015-11 |
PubMed番号: | 26370682 |
関連ページ: | http://doi.org/10.5387/fms.2015-11 |
権利情報: | © 2015 The Fukushima Society of Medical Science |
出現コレクション: | Vol.61 (2015)
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