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ER stress suppresses DNA double-strand break repair and sensitizes tumor cells to ionizing radiation by stimulating proteasomal degradation of Rad51

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/53269

Title: ER stress suppresses DNA double-strand break repair and sensitizes tumor cells to ionizing radiation by stimulating proteasomal degradation of Rad51
Authors: Yamamori, Tohru Browse this author →KAKEN DB
Meike, Shunsuke Browse this author
Nagane, Masaki Browse this author
Yasui, Hironobu Browse this author →KAKEN DB
Inanami, Osamu Browse this author →KAKEN DB
Keywords: ER stress
Rad51
DNA double-strand break repair
Radiosensitivity
Unfolded protein response
Issue Date: 11-Oct-2013
Publisher: Elsevier
Journal Title: FEBS Letters
Volume: 587
Issue: 20
Start Page: 3348
End Page: 3353
Publisher DOI: 10.1016/j.febslet.2013.08.030
PMID: 24021650
Abstract: In this study, we provide evidence that endoplasmic reticulum (ER) stress suppresses DNA double-strand break (DSB) repair and increases radiosensitivity of tumor cells by altering Rad51 levels. We show that the ER stress inducer tunicamycin stimulates selective degradation of Rad51 via the 26S proteasome, impairing DSB repair and enhancing radiosensitivity in human lung cancer A549 cells. We also found that glucose deprivation, which is a physiological inducer of ER stress, triggered similar events. These findings suggest that ER stress caused by the intratumoral environment influences tumor radiosensitivity, and that it has potential as a novel target to improve cancer radiotherapy.
Type: article (author version)
URI: http://hdl.handle.net/2115/53269
Appears in Collections:獣医学院・獣医学研究院 (Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 山盛 徹

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