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Abstract
The role of end-binding protein 1 (EB1) in lung cancer tumorigenesis and radiotherapy remains poorly understood. In the present study, we observed that EB1 was highly expressed in lung tumor tissues compared with normal non-tumor tissues based on immunohistochemical analysis of lung cancer tissue samples obtained from human tissue microarrays. EB1 was also highly overexpressed in radioresistant lung and cervical cancer cells, which exhibited increased cell death after EB1 silencing. The cytotoxicity induced by EB1 gene knockdown was due to the activation and generation of reactive oxygen species by p38 mitogen-activated protein kinase. Notably, this signaling cascade, however not nuclear factor-κB-mediated signaling, induced the expression of cyclooxygenase-2, a key effector of apoptotic death. Our results provided new molecular evidence supporting the use of EB1 as a novel target in lung cancer therapy, especially in the case of radioresistance.

Author information

Baek JH1, Yim JH1, Song JY1, Um HD1, Park JK1, Park IC1, Kim JS1, Lee CW2, Hong EH3, Kim EH1, Hwang SG1.
1
Division of Applied Radiation Bioscience, Korea Institute of Radiological and Medical Sciences, Seoul 01812, Republic of Korea.
2
Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon 440-746, Republic of Korea.
3
Low-dose Radiation Research Team, Korea Hydro and Nuclear Power, Seoul 01450, Republic of Korea.