Study of P14/ARF Gene Promoter Methylation and Effect of Interleukin-17 Gene Polymorphism on this Methylation among Breast Cancer Patients
Background: hyper-methylation in CpG Island is one of the major mechanisms in gene silencing. In many cancers, different genes are experiencing CIHM (CpG island hyper methylation). P14 / ARF regulatory factor, involved in negative regulation of the cell cycle through the effect on P53 factor pathway...
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Veröffentlicht in: | Ṭibb-i junūb 2016-11, Vol.19 (5), p.809-818 |
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Sprache: | eng ; per |
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Zusammenfassung: | Background: hyper-methylation in CpG Island is one of the major mechanisms in gene silencing. In many cancers, different genes are experiencing CIHM (CpG island hyper methylation). P14 / ARF regulatory factor, involved in negative regulation of the cell cycle through the effect on P53 factor pathway. On the other hand, Interleukin 17 can be increased methylation by inflammatory effects. The purpose of this study was to study the P14/ARF gene promoter methylation and effect of Interleukin-17 on this methylation among breast cancer patients in the south of the country and its comparison with healthy people. Materials and Methods: in this case-control study, peripheral blood of 40 patients with breast cancer who were referred to hospitals in Shiraz and 40 healthy women was used to DNA extraction by using salt out and K proteinase . Control subjects with a family history of cancer or autoimmune diseases were excluded from the study. We used PCR-RFLP method In order to study of Interleukin-17 gene polymorphism, and MSPCR method was used to study of P14/ARF gene promoter methylation. The results of the study were studied by using SPSS software, Arlequin, chi-square and Hardy-weinberg equilibrium test was used respectively. Results: findings confirms that there was a significant association between P14/ARF gene promoter methylation and disease and mentioned gene promoter was less methylated in healthy subjects compared to patients (p |
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ISSN: | 1735-4374 1735-6954 |
DOI: | 10.18869/acadpub.ismj.19.5.809 |