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Vol.61 (2015) >

Please use this identifier to cite or link to this item: http://ir.fmu.ac.jp/dspace/handle/123456789/489

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Title: Overexpression of both CLOCK and BMAL1 inhibits entry to S phase in human colon cancer cells
Authors: Sakamoto, Wataru
Takenoshita, Seiichi
Affiliation: 器官制御外科学講座
Source title: Fukushima Journal of Medical Science
Volume: 61
Issue: 2
Start page: 111
End page: 124
Issue Date: 2015
Abstract: 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.
Publisher: The Fukushima Society of Medical Science
Publisher (Alternative foam): 福島医学会
language: eng
URI: http://ir.fmu.ac.jp/dspace/handle/123456789/489
Full text 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 ID: 26370682
Related Page: http://doi.org/10.5387/fms.2015-11
Rights: © 2015 The Fukushima Society of Medical Science
Appears in Collections:Vol.61 (2015)

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