Alteration of Apurinic/Apyrimidinic Endonuclease-1/Redox Factor-1 in Human Non-small Cell Lung Cancer.
- Author:
Dae Goon YOO
1
;
Yun Jeong SONG
;
Eun Jung CHO
;
Min Woong KANG
;
Jong Hee HAN
;
Myung Hoon NA
;
Seung Pyung LIM
;
Jae Hyeon YU
;
Byeong Hwa JEON
;
Young LEE
Author Information
1. Department of Physiology, College of Medicine, Chungnam National University, Korea.
- Publication Type:Original Article
- Keywords:
Lung neoplasms;
Proteins
- MeSH:
Antibodies;
Antioxidants;
Blotting, Western;
Carcinoma, Non-Small-Cell Lung*;
Catalase;
Cytoplasm;
DNA;
DNA Repair;
Humans*;
Lung;
Lung Neoplasms;
Oxidants;
Oxidation-Reduction;
Oxidative Stress;
Transcription Factors
- From:The Korean Journal of Thoracic and Cardiovascular Surgery
2007;40(8):529-535
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: An imbalance between oxidants and antioxidants leads to oxidative stress, and this has been proposed to play an important role in the pathogenesis of lung neoplasm. Apurinic/apyrimidinic endonuclease-1/redox factor-1 (APE/ref-1) is a multifunctional protein involved in DNA base excision repair and the redox regulation of many transcription factors. However, the alteration of the expressed levels of APE/ref-1 in non-small cell lung cancer is unknown. MATERIAL AND METHOD: Forty-nine patients with surgically resected non-small cell lung cancer (NSCLC) were included in this study. Immunohistochemical staining with APE/ref-1 antibodies was performed, and their expressions were analyzed via Western blotting for specific antibodies. RESULT: APE/ref-1 was localized at the nucleus and mainly in the non-tumor region of the NSCLC tissue specimens; it was expressed in the cytoplasm and nucleus of the NSCLC. The nuclear and cytoplasmic expressions of APE/ref-1 in lung cancers were markedly up-regulated in the NSCLC, and this was correlated with the clinical stage. Catalase, as first-line antioxidant defense, was dramatically decreased in the NSCLC. CONCLUSION: Taken together, our results suggest that APE/ref-1, and especially cytoplasmic APE/ref-1, was upregulated in the lung cancer regions, and this may contribute to the compensatory defense system against oxidative stress. A low expression of catalase might have fundamental effects on the extracellular redox state of lung tumors, along with the potential consequences for the tumors.
