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

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 Lett

journal_title

FEBS letters

authors

Yamamori T,Meike S,Nagane M,Yasui H,Inanami O

doi

10.1016/j.febslet.2013.08.030

subject

Has Abstract

pub_date

2013-10-11 00:00:00

pages

3348-53

issue

20

eissn

0014-5793

issn

1873-3468

pii

S0014-5793(13)00659-5

journal_volume

587

pub_type

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