作者: Eun Sang Lee , Hae-June Lee , Yoon-Jin Lee , Jae-Hoon Jeong , Seongman Kang
DOI: 10.1016/J.BBRC.2014.06.091
关键词:
摘要: Radiotherapy, which is one of the most effective approaches to treatment various cancers, plays an important role in malignant cell eradication pelvic area and abdomen. However, it also generates some degree intestinal injury. Apoptosis epithelium primary pathological factor that initiates radiation-induced injury, but mechanism by ionizing radiation (IR) induces apoptosis not clearly understood. Recently, IR has been shown induce endoplasmic reticulum (ER) stress, thereby activating unfolded protein response (UPR) signaling pathway epithelial cells. consequences IR-induced activation UPR on radiosensitivity cells remain be determined. In this study, we investigated ER stress responses death. We show chemical inducers, such as tunicamycin or thapsigargin, enhanced caspase 3 DNA fragmentation Knockdown Xbp1 Atf6 with small interfering RNA inhibited activation. Treatment chaperones prevented subsequent IR-exposed Our results suggest a pro-apoptotic Furthermore, inhibiting may strategy prevent