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

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.

収録刊行物

• FEBS Letters

  FEBS Letters 587 (20), 3348-3353, 2013-10-11

  Elsevier

キーワード

• ER stress
• Rad51
• DNA double-strand break repair
• Radiosensitivity
• Unfolded protein response

詳細情報

• CRID: 1050282677651766016
• NII論文ID: 120005326756
• NII書誌ID: AA00642943
• HANDLE: 2115/53269
• ISSN: 00145793
• 本文言語コード: en
• 資料種別: journal article
• データソース種別:
  • IRDB
  • CiNii Articles