Abstract
BackgroundAPE1 (apurinic/apyrimidinic endonuclease 1) is an important DNA repair protein in the base excision repair pathway. Polymorphisms in APE1 have been implicated in susceptibility to cancer; however, results from the published studies remained inconclusive. The objective of this study was to conduct a meta-analysis investigating the association between polymorphisms in APE1 and the risk for cancer.MethodsThe PubMed and Embase databases were searched for case-control studies published up to June, 2011 that investigated APE1 polymorphisms and cancer risk. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to assess the strength of the associations.ResultsTwo polymorphisms (−656 T > G, rs1760944 and 1349 T > G, rs1130409) in 37 case-control studies including 15, 544 cancer cases and 21, 109 controls were analyzed. Overall, variant genotypes (GG and TG/GG) of −656 T > G polymorphism were associated with significantly decreased cancer risk in homozygote comparison (OR = 0.81, 95%CI: 0.67-0.97), dominant model comparison (OR = 0.89, 95%CI: 0.81-0.97) and recessive model comparison (OR = 0.90, 95%CI: 0.82-0.98), whereas the 1349 T > G polymorphism had no effects on overall cancer risk. In the stratified analyses for −656 T > G polymorphism, there was a significantly decreased risk of lung cancer and among Asian populations.ConclusionsAlthough some modest bias could not be eliminated, the meta-analysis suggests that APE1 −656 T > G polymorphism has a possible protective effect on cancer risk particularly among Asian populations whereas 1349 T > G polymorphism does not contribute to the development of cancer.
Highlights
APE1 is an important DNA repair protein in the base excision repair pathway
Studies that were included in the meta-analysis had to meet all of the following criteria: 1) evaluate the APE1 −656T > G and 1349T > G polymorphisms and cancer risk, 2) use a case-control design, 3) contain available genotypes frequency for estimating an odds ratio (OR) with a 95% confidence intervals (CIs), 4) genotype distributions in control consistent with HardyWeinberg equilibrium (HWE)
We examined the association between the APE1 −656 T > G and 1349 T > G polymorphisms and cancer risk in homozygote comparison (GG vs. TT), heterozygote comparison (TG vs. TT), the dominant genetic model (TG/GG vs. TT), and the recessive genetic model (GG vs. TT/TG)
Summary
APE1 (apurinic/apyrimidinic endonuclease 1) is an important DNA repair protein in the base excision repair pathway. The incidence of different cancer varies widely in different populations which may be largely attributed to lifestyle and genetic background [2]. Environmental factors such as smoking and exposure to carcinogens lead to direct damage to DNA [3]. Among DNA repair systems, base excision repair (BER) pathway is responsible for repairing small lesions such as oxidative damage, alkylation, or methylation [5]. APE1 can act as a 3’-phosphodiesterase to initiate repair of DNA single strand breaks, which are produced either directly by reactive oxygen species or indirectly through the enzymatic removal of damaged bases [7,8]. APE1 is known as a transcriptional coactivator for numerous transcription factors involved in cancer development [9] and is considered as a promising tool for anticancer therapy [10]
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