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Hokkaido University Collection of Scholarly and Academic Papers >
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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
| 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)
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Submitter: 山盛 徹
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