The Association between CA Polymorphism in src Gene and Risk of Breast Cancer

Document Type : Original Article (s)

Authors

1 Department of Biology, School of Science, University of Isfahan, Isfahan, Iran

2 Professor, Department of Biology, School of Science, University of Isfahan, Isfahan, Iran

3 Assistant Professor, Department of Radiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

Abstract

Background: Breast cancer is the most common malignancy in women and is the first cause of death among the women in the world. Disruption of gene expression of src family members has been observed in many cancers. Repeated sequences in introns influence gene expression, splicing or change the structure of product. In the present study, the association between CA polymorphism in intron 2 of the src gene and the risk of breast cancer was investigated.Methods: This was a cohort study on 119 patients with breast cancer and 145 healthy people. Genomic DNAs were extracted from white blood cells. CA dinucleotide region of the src gene was amplified via polymerase chain reaction (PCR) technique and the number of CA repeats was determined using polyacrylamide gel electrophoresis.Findings: Distribution of the CA repeats in src gene in the target population was between 14-27 repeats. The most common allele in two groups was 21. The frequency of the allele 22 in patients was significantly higher than healthy group. 26 genotypes were identified and the genotype 21/21 was the most common one among the two groups. The genotype 22/22 was more frequent in patients than in healthy group. Chi-square test and odds ratio (OR) showed that women with allele 22 were exposed more to breast cancer. Women with genotype 22/22 had a higher risk of developing breast cancer.Conclusion: it can be concluded that the allele 22 can have a role in developing breast cancer.

Keywords

References

  1. Planas-Silva MD, Bruggeman RD, Grenko RT, Stanley SJ. Role of c-Src and focal adhesion kinase in progression and metastasis of estrogen receptor-positive breast cancer. Biochem Biophys Res Commun 2006; 341(1): 73-81.
  2. Benson JR, Jatoi I. The global breast cancer burden. Future Oncol 2012; 8(6): 697-702.
  3. Zhang S, Yu D. Targeting Src family kinases in anti-cancer therapies: turning promise into triumph. Trends Pharmacol Sci 2012; 33(3): 122-8.
  4. Elsberger B. Translational evidence on the role of Src kinase and activated Src kinase in invasive breast cancer. Crit Rev Oncol Hematol 2014; 89(3): 343-51.
  5. Beristain AG, Molyneux SD, Joshi PA, Pomroy NC, Di Grappa MA, Chang MC, et al. PKA signaling drives mammary tumorigenesis through Src. Oncogene 2015; 34(9): 1160-73.
  6. Sanchez-Bailon MP, Calcabrini A, Mayoral-Varo V, Molinari A, Wagner KU, Losada JP, et al. Cyr61 as mediator of Src signaling in triple negative breast cancer cells. Oncotarget 2015; 6(15): 13520-38.
  7. Jarne P, Lagoda PJ. Microsatellites, from molecules to populations and back. Trends Ecol Evol 1996; 11(10): 424-9.
  8. Herold CI, Chadaram V, Peterson BL, Marcom PK, Hopkins J, Kimmick GG, et al. Phase II trial of dasatinib in patients with metastatic breast cancer using real-time pharmacodynamic tissue biomarkers of Src inhibition to escalate dosing. Clin Cancer Res 2011; 17(18): 6061-70.
  9. Lian Y, Garner HR. Evidence for the regulation of alternative splicing via complementary DNA sequence repeats. Bioinformatics 2005; 21(8): 1358-64.
  10. Hegyi H, Kalmar L, Horvath T, Tompa P. Verification of alternative splicing variants based on domain integrity, truncation length and intrinsic protein disorder. Nucleic Acids Res 2011; 39(4): 1208-19.
  11. Lim HT, Zhong T, Cho IC, Seo BY, Kim JH, Lee SS, et al. Novel alternative splicing by exon skipping in KIT associated with whole-body roan in an intercrossed population of Landrace and Korean Native pigs. Anim Genet 2011; 42(4): 451-5.
Journal of Isfahan Medical School
Volume 35, Issue 419 - Serial Number 419
January and February 2017
Pages 87-92

Files

History

  • Receive Date: 07 December 2016
  • Revise Date: 01 November 2024
  • Accept Date: 06 April 2022

Share

How to cite

Statistics