Chemical chaperones reduce ionizing radiation-induced endoplasmic reticulum stress and cell death in IEC-6 cells

Eun Sang Lee, Hae June Lee, Yoon Jin Lee, Jae Hoon Jeong, Seongman Kang, Young Bin Lim

Research output: Contribution to journalArticlepeer-review

17 Citations (Scopus)


Radiotherapy, which is one of the most effective approaches to the treatment of various cancers, plays an important role in malignant cell eradication in the pelvic area and abdomen. However, it also generates some degree of intestinal injury. Apoptosis in the intestinal epithelium is the primary pathological factor that initiates radiation-induced intestinal injury, but the mechanism by which ionizing radiation (IR) induces apoptosis in the intestinal epithelium is not clearly understood. Recently, IR has been shown to induce endoplasmic reticulum (ER) stress, thereby activating the unfolded protein response (UPR) signaling pathway in intestinal epithelial cells. However, the consequences of the IR-induced activation of the UPR signaling pathway on radiosensitivity in intestinal epithelial cells remain to be determined. In this study, we investigated the role of ER stress responses in IR-induced intestinal epithelial cell death. We show that chemical ER stress inducers, such as tunicamycin or thapsigargin, enhanced IR-induced caspase 3 activation and DNA fragmentation in intestinal epithelial cells. Knockdown of Xbp1 or Atf6 with small interfering RNA inhibited IR-induced caspase 3 activation. Treatment with chemical chaperones prevented ER stress and subsequent apoptosis in IR-exposed intestinal epithelial cells. Our results suggest a pro-apoptotic role of ER stress in IR-exposed intestinal epithelial cells. Furthermore, inhibiting ER stress may be an effective strategy to prevent IR-induced intestinal injury.

Original languageEnglish
Pages (from-to)1005-1009
Number of pages5
JournalBiochemical and biophysical research communications
Issue number2
Publication statusPublished - 2014 Jul 25

Bibliographical note

Funding Information:
This study was supported by the Nuclear Research and Development Program of the National Research Foundation of Korea, which was funded by the Korean government ( Ministry of Education, Science, and Technology ; grant code: 50034-2014 and 2013M2A2A7043580 ).


  • Chemical chaperone
  • Endoplasmic reticulum stress
  • Ionizing radiation
  • Unfolded protein response

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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