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.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Yamamori T,Meike S,Nagane M,Yasui H,Inanami Odoi
10.1016/j.febslet.2013.08.030subject
Has Abstractpub_date
2013-10-11 00:00:00pages
3348-53issue
20eissn
0014-5793issn
1873-3468pii
S0014-5793(13)00659-5journal_volume
587pub_type
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