Expression and promoter-hyper methylation analysis of MGMT gene in patients with pterygium

2019 
1) Background: Pterygium is a benign legion and is observed as aggressive growth of conjunctiva fibro-vascular tissue on the cornea. The alkylating agents are observed as considerable threats for human health because alkylated lesions lead to cytotoxic, teratogenic and cancerizing effects. MGMT is one of the repair proteins of DNA which repairs the alkylated lesions. Expression and activity of MGMT is controlled by epigenetic mechanisms such as DNA methylation in the promoter regions like transcription factors which are connected to MGMT promoter and lead to positive or negative induction of that activity, protein-protein interactions, and negative regulation. 2) Materials and methods: In order to study methylation, DNA samples of 43 patients and 40 healthy individuals were extracted, bisulfited and then were studied. Also in order to study the expression, RNA was extracted from 15 other patients and 15 other healthy individuals; and then, the technique of Real-time PCR was used. 3) Results: analysis of promoter methylation of MGTM gene showed that there is no significant relationship in the situation of promoter methylation between the patients and control individuals (P value = 0.43; 95%Cl = 0.66-2.40; OR = 1.52). However, analysis of MGMT gene expression showed significant difference between the patients and control individuals (Mean ± SD: 1.25 ± 0.10 and 1.52 ± 2.91, respectively; P value = 0.009). 4) Conclusion: since there are no significant changes of promoter methylation of MGMT gene, there seems to be other unknown procedures that regulate this gene’s expression levels. In this respect, expression of MGMT gene in the pterygium increases through unknown procedures. In order to approve this data, further studies are suggested in more populations with bigger sample sizes by the use of advanced molecular techniques.
    • Correction
    • Source
    • Cite
    • Save
    • Machine Reading By IdeaReader
    0
    References
    0
    Citations
    NaN
    KQI
    []