RESEARCH COMMUNICATION Association Between the Ku70 -1310C/G Promoter Polymorphism and Cancer Risk: a Meta-analysis

By affecting genomic stability, DNA damage may induce abnormal cell proliferation, differentiation and apoptosis, which finally leads to carcinogenesis. As the major opponent of genetic injury, DNA repair mechanisms are essential in preventing tumor initiation and progress (Shiraishi et al., 2010). DNA double-strand breaks (DSB) are the most serious type of DNA damage (Wood et al., 2001) that can be repaired by DNA DSB repair system. DNA DSB repair system consists of two sub-pathways, among which nonhomologous end-joining (NHEJ) is predominant in humans (Khanna and Jackson, 2001). The central factor of NHEJ is DNA-dependent protein kinase (DNA-PK), composed of DNA-PK catalytic subunit (DNA-PKcs) and Ku70/Ku80 heterodimer (Pfeiffer et al., 2000). Ku70, the product of the Ku70 gene (also named XRCC6 gene), is proposed to be a caretaker protein, which suppresses chromosomal rearrangements and maintains genome integrity (Tseng et al., 2009). A potentially functional polymorphism in the promoter region of Ku70 is described as -1310C/G (rs2267437) (Sobczuk et al., 2010). Various case-control studies have investigated the association between the risk of human cancer and Ku70 -1310C/G promoter polymorphism; however, the findings have been conflicting. Furthermore, due to limitations in