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World J Gastroenterol. Oct 28, 2013; 19(40): 6894-6901
Published online Oct 28, 2013. doi: 10.3748/wjg.v19.i40.6894
Published online Oct 28, 2013. doi: 10.3748/wjg.v19.i40.6894
Abnormal DNA-PKcs and Ku 70/80 expression may promote malignant pathological processes in gastric carcinoma
Wei Li, Chuan Xie, Zhen Yang, Jiang Chen, Nong-Hua Lu, Department of Gastroenterology, the First Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi Province, China
Author contributions: Li W and Lu NH designed the study; Xie C, Yang Z and Chen J performed the experiments; Li W analyzed the data; Li W and Lu NH drafted the manuscript.
Supported by The National natural science foundation of China, No. 81270479
Correspondence to: Nong-Hua Lu, MD, Department of Gastroenterology, the First Affiliated Hospital of Nanchang University, Yongzheng Road, Donghu District, Nanchang 330006, Jiangxi Province, China. lunonghua@ncu.edu.cn
Telephone: +86-791-88692705 Fax: +86-791-88623153
Received: May 11, 2013
Revised: September 4, 2013
Accepted: September 15, 2013
Published online: October 28, 2013
Revised: September 4, 2013
Accepted: September 15, 2013
Published online: October 28, 2013
Core Tip
Core tip: This is the first study to clarify the two key promoters of the non-homologous end joining (NHEJ) pathway, DNA-dependent protein kinase (DNA-PKcs) and Ku 70/80, in human gastric carcinoma tissues. The present study found an upregulated expression of DNA-PKcs and Ku 70/80 in gastric cancer tissues compared with normal gastric mucosa, which suggests that there is an enhanced function of NHEJ in gastric carcinogenesis. As NHEJ is an error-prone and non-specific repair mechanism and can be induced before homologous recombination, its excessive activation is capable of regulating cell cycle arrest, cell apoptosis, chromosome recombination and genome instability.