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Lack of Association Between LIG4 Gene Polymorphisms and the Risk of Breast Cancer: A HuGE Review and Meta-analysis

  • Zhou, Li-Ping (Department of Laboratory Medicine, the First Affiliated Hospital of China Medical University) ;
  • Luan, Hong (Department of Laboratory Medicine, the First Affiliated Hospital of China Medical University) ;
  • Dong, Xi-Hua (Department of Laboratory Medicine, the First Affiliated Hospital of China Medical University) ;
  • Jin, Guo-Jiang (Department of Laboratory Medicine, the First Affiliated Hospital of China Medical University) ;
  • Man, Dong-Liang (Department of Laboratory Medicine, the First Affiliated Hospital of China Medical University) ;
  • Shang, Hong (Department of Laboratory Medicine, the First Affiliated Hospital of China Medical University)
  • Published : 2012.07.31

Abstract

Objective: Non-homologous end joining (NHEJ) is one of the pathways of repair of DNA double-strand breaks. A number of genes involved in NHEJ have been implicated as breast cancer susceptibility genes such as LIG4. However, some studies have generated conflicting results. The aim of this Human Genome Epidemiology (HuGE) review and meta-analysis was to investigate association between LIG4 gene polymorphisms in the NHEJ pathway and breast cancer risk. Methods: Studies focusing on the relationship between LIG4 gene polymorphisms and susceptibility to breast cancer were selected from the Pubmed, Cochrane library, Embase, Web of Science, Springerlink, CNKI and CBM databases. Data were extracted by two independent reviewers and the meta-analysis was performed with Review Manager Version 5.1.6 and STATA Version 12.0 software, calculating odds ratios (ORs) with 95% confidence intervals (95%CIs). Results: According to the inclusion criteria, we final included seven studies with a total of 10,321 breast cancer cases and 10,160 healthy controls in the meta-analysis. The results showed no association between LIG4 gene polymorphisms (rs1805386 T>C, rs1805389 C>T, rs1805388 C>T and rs2232641 A>G) and breast cancer risk, suggesting that the mutant situation of these SNPs neither increased nor decreased the risk for breast cancer. In the subgroup analysis by Hardy-Weinberg equilibrium (HWE) and ethnicity, we also found no associations between the variants of LIG4 gene and breast cancer risk among HWE, non-HWE, Caucasians, Asians and Africans. Conclusion: This meta-analysis suggests that there is a lack of any association between LIG4 gene polymorphisms and the risk of breast cancer.

Keywords

References

  1. Acevedo N, Mercado D, Vergara C, et al (2009). Association between total immunoglobulin E and antibody responses to naturally acquired Ascaris lumbricoides infection and polymorphisms of immune system-related LIG4, TNFSF13B and IRS2 genes. Clin Exp Immunol, 157, 282-90. https://doi.org/10.1111/j.1365-2249.2009.03948.x
  2. Balmain A, Gray J, Ponder B (2003). The genetics and genomics of cancer. Nat Genet, 33 (Suppl), 238-44. https://doi.org/10.1038/ng1107
  3. Breast Cancer Association Consortium (2006). Commonly studied single-nucleotide polymorphisms and breast cancer: results from the Breast Cancer Association Consortium. J Natl Cancer Inst, 98, 1382-96. https://doi.org/10.1093/jnci/djj374
  4. Cao AY, Huang J, Hu Z, et al (2009). Mutation analysis of BRIP1/BACH1 in BRCA1/BRCA2 negative Chinese women with early onset breast cancer or affected relatives. Breast Cancer Res Treat, 115, 51-5. https://doi.org/10.1007/s10549-008-0052-z
  5. Dapic V, Carvalho MA, Monteiro AN (2005). Breast cancer susceptibility and the DNA damage response. Cancer Control, 12, 127-136.
  6. Ferguson DO, Alt FW. (2001) DNA double strand break repair and chromosomal translocation: lessons from animal models. Oncogene, 20, 5572-9. https://doi.org/10.1038/sj.onc.1204767
  7. Frank-Vaillant M, Marcand S (2001). NHEJ regulation by mating type is exercised through a novel protein, Lif2p, essential to the ligase IV pathway. Genes Dev, 15, 3005-12. https://doi.org/10.1101/gad.206801
  8. Fu YP, Yu JC, Cheng TC, et al (2003). Breast cancer risk associated with genotypic polymorphism of the nonhomologous end-joining genes: a multigenic study on cancer susceptibility. Cancer Res, 63, 2440-6.
  9. Garcia AM, Salomon RN, Witsell A, et al (2011). Loss of the bloom syndrome helicase increases DNA ligase 4-independent genome rearrangements and tumorigenesis in aging Drosophila. Genome Biol, 12, R121. https://doi.org/10.1186/gb-2011-12-12-r121
  10. Garcia-Closas M, Egan KM, Newcomb PA, et al (2006). Polymorphisms in DNA double-strand break repair genes and risk of breast cancer: two population-based studies in USA and Poland, and meta-analyses. Hum Genet, 119, 376-88. https://doi.org/10.1007/s00439-006-0135-z
  11. Goode EL, Dunning AM, Kuschel B, et al (2002). Effect of germ-line genetic variation on breast cancer survival in a population-based study. Cancer Res, 62, 3052-7.
  12. Grabarz A, Barascu A, Guirouilh-Barbat J, et al (2012). Initiation of DNA double strand break repair: signaling and single-stranded resection dictate the choice between homologous recombination, non-homologous end-joining and alternative end joining. Am J Cancer Res, 2, 249-68.
  13. Han J, Hankinson SE, Ranu H, et al (2004). Polymorphisms in DNA double-strand break repair genes and breast cancer risk in the Nurses' Health Study. Carcinogenesis, 25, 189-95.
  14. Henrique Barreta M, Garziera Gasperin B, Braga Rissi V, et al (2012). Homologous recombination and non-homologous end-joining repair pathways in bovine embryos with different developmental competence. Exp Cell Res, (in press).
  15. Higgins JP, Thompson SG (2002). Quantifying heterogeneity in a meta-analysis. Stat Med, 21, 1539-58. https://doi.org/10.1002/sim.1186
  16. Hsu HM, Wang HC, Chen ST, et al (2007) Breast cancer risk is associated with the genes encoding the DNA double-strand break repair Mre11/Rad50/Nbs1 complex. Cancer Epidemiol Biomarkers Prev, 16, 2024-32. https://doi.org/10.1158/1055-9965.EPI-07-0116
  17. Jakubowska A, Gronwald J, Menkiszak J, et al (2010). BRCA1-associated breast and ovarian cancer risks in Poland: no association with commonly studied polymorphisms. Breast Cancer Res Treat, 119, 201-11. https://doi.org/10.1007/s10549-009-0390-5
  18. Kapusta A, Matsuda A, Marmignon A, et al (2011) Highly precise and developmentally programmed genome assembly in Paramecium requires ligase IV-dependent end joining. PLoS Genet, 7, e1002049. https://doi.org/10.1371/journal.pgen.1002049
  19. Kuschel B, Auranen A, McBride S, et al (2002). Variants in DNA double-strand break repair genes and breast cancer susceptibility. Hum Mol Genet, 11, 1399-407. https://doi.org/10.1093/hmg/11.12.1399
  20. Lacey JV Jr, Devesa SS, Brinton LA (2002). Recent trends in breast cancer incidence and mortality. Environ Mol Mutagen, 39, 82-8. https://doi.org/10.1002/em.10062
  21. Li Z, Luo Y, Gong Y, et al (2011). Clinical features and molecular phenotypes of breast cancer in patients with type-2 diabetes mellitus. Asian Pac J Cancer Prev, 12, 2183-8.
  22. Liang L, Deng L, Nguyen SC, et al (2008). Human DNA ligases I and III, but not ligase IV, are required for microhomology-mediated end joining of DNA double-strand breaks. Nucleic Acids Res, 36, 3297-310. https://doi.org/10.1093/nar/gkn184
  23. Mahaney BL, Meek K, Lees-Miller SP (2009). Repair of ionizing radiation-induced DNA double-strand breaks by non-homologous end-joining. Biochem J, 417, 639-50. https://doi.org/10.1042/BJ20080413
  24. Mao Z, Bozzella M, Seluanov A, et al (2008). DNA repair by nonhomologous end joining and homologous recombination during cell cycle in human cells. Cell Cycle, 7, 2902-6. https://doi.org/10.4161/cc.7.18.6679
  25. Matullo G, Dunning AM, Guarrera S, et al (2006) DNA repair polymorphisms and cancer risk in non-smokers in a cohort study. Carcinogenesis, 27, 997-1007. https://doi.org/10.1093/carcin/bgi280
  26. Monsees GM, Kraft P, Chanock SJ, et al (2011) Comprehensive screen of genetic variation in DNA repair pathway genes and postmenopausal breast cancer risk. Breast Cancer Res Treat, 125, 207-14. https://doi.org/10.1007/s10549-010-0947-3
  27. Okoh V, Deoraj A, Roy D (2011). Estrogen-induced reactive oxygen species-mediated signalings contribute to breast cancer. Biochim Biophys Acta, 1815, 115-33.
  28. Parkin DM, Bray F, Ferlay J, et al (2001). Estimating the world cancer burden: Globocan 2000. Int J Cancer, 94, 153-6. https://doi.org/10.1002/ijc.1440
  29. Pastwa E, Błasiak J (2003). Non-homologous DNA end joining. Acta Biochim Pol, 50, 891-908.
  30. Peters JL, Sutton AJ, Jones DR, et al (2006). Comparison of two methods to detect publication bias in meta-analysis. JAMA, 295, 676-80. https://doi.org/10.1001/jama.295.6.676
  31. Peto J, Collins N, Barfoot R, et al (1999). Prevalence of BRCA1 and BRCA2 gene mutations in patients with early-onset breast cancer. J Natl Cancer Inst, 91, 943-9. https://doi.org/10.1093/jnci/91.11.943
  32. Ponder BA (2001). Cancer genetics. Nature, 411, 336-41. https://doi.org/10.1038/35077207
  33. Rafii S, O'Regan P, Xinarianos G, et al (2002). A potential role for the XRCC2 R188H polymorphic site in DNA-damage repair and breast cancer. Hum Mol Genet, 11, 1433-8. https://doi.org/10.1093/hmg/11.12.1433
  34. Rothkamm K, Kruger I, Thompson LH, et al (2003) Pathways of DNA double-strand break repair during the mammalian cell cycle. Mol Cell Biol, 23, 5706-15. https://doi.org/10.1128/MCB.23.16.5706-5715.2003
  35. Shrivastav M, De Haro LP, Nickoloff JA (2008). Regulation of DNA double-strand break repair pathway choice. Cell Res, 18, 134-47. https://doi.org/10.1038/cr.2007.111
  36. Symington LS, Gautier J (2011). Double-strand break end resection and repair pathway choice. Annu Rev Genet, 45, 247-71. https://doi.org/10.1146/annurev-genet-110410-132435
  37. Venkitaraman AR (2002). Cancer susceptibility and the functions of BRCA1 and BRCA2. Cell, 108, 171-82. https://doi.org/10.1016/S0092-8674(02)00615-3
  38. von Elm E, Altman DG, Egger M, et al (2007). The Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) statement: guidelines for reporting observational studies. Lancet, 370, 1453-7. https://doi.org/10.1016/S0140-6736(07)61602-X
  39. Wang HX, Ying MZ, Wang YJ (2012). Association of DNA double strand break repair pathway and hereditary breast cancer. Chin Clin Oncol, 17, 267-71.
  40. Wernberg JA, Yap J, Murekeyisoni C, et al (2009). Multiple primary tumors in men with breast cancer diagnoses: a SEER database review. J Surg Oncol, 99, 16-9. https://doi.org/10.1002/jso.21153
  41. Yano K, Morotomi-Yano K, Adachi N, et al (2009). Molecular mechanism of protein assembly on DNA double-strand breaks in the non-homologous end-joining pathway. J Radiat Res, 50, 97-108. https://doi.org/10.1269/jrr.08119
  42. Yoshida K, Miki Y (2004). Role of BRCA1 and BRCA2 as regulators of DNA repair, transcription, and cell cycle in response to DNA damage. Cancer Sci, 95, 866-71. https://doi.org/10.1111/j.1349-7006.2004.tb02195.x
  43. Zhang L, Liu JL, Zhang YJ, et al (2011). Association between $HLA-B^\ast27$ polymorphisms and ankylosing spondylitis in Han populations: a meta-analysis. Clin Exp Rheumatol, 29, 285-92.
  44. Zintzaras E, Ioannidis JP (2005). Heterogeneity testing in meta-analysis of genome searches. Genet Epidemiol, 28, 123-37. https://doi.org/10.1002/gepi.20048

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