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

Yamamori, Tohru; Meike, Shunsuke; Nagane, Masaki; Yasui, Hironobu; Inanami, Osamu

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

Yamamori, Tohru; Meike, Shunsuke; Nagane, Masaki et al.

FEBS Letters, 2013, 587(20), 3348-3353

Permalink : https://hdl.handle.net/2115/53269

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論文情報

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アクセス権	open access
URI	https://hdl.handle.net/2115/53269
タイトル	ER stress suppresses DNA double-strand break repair and sensitizes tumor cells to ionizing radiation by stimulating proteasomal degradation of Rad51
著者	Yamamori, Tohru ; Meike, Shunsuke ; Nagane, Masaki ; Yasui, Hironobu ; Inanami, Osamu
e-Rad_Researcher 00512675 著者名 Yamamori, Tohru
著者名 Meike, Shunsuke
著者名 Nagane, Masaki
e-Rad_Researcher 10570228 著者名 Yasui, Hironobu
e-Rad_Researcher 10193559 著者名 Inanami, Osamu
言語	英語
キーワード	ER stress
	Rad51
	DNA double-strand break repair
	Radiosensitivity
	Unfolded protein response
発行日	2013-10-11
出版者	Elsevier
収録物名	FEBS Letters
巻(号)	587(20)
ページ	3348-3353
抄録	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.
資源タイプ	学術雑誌論文
出版タイプ	Accepted Manuscript
PISSN	0014-5793
NCID	AA00642943
関連情報	PMID 24021650
関連情報 (isVersionOf)	出版社版DOI https://doi.org/10.1016/j.febslet.2013.08.030