Association of Human Methionine Synthase-A2756G Transition With Prostate Cancer: A Case-Control Study and in Silico

Arezou Ebrahimi1, Abasalt Hosseinzadeh Colagar2, Mohammad Karimian3

  • 1Department of Biology, Faculty of Sciences, Islamic Azad University, Damghan Branch, Damghan, Iran. AND Department of Molecular and Cell Biology, Faculty of Basic Sciences, University of Mazandaran, Babolsar, Iran.

Acta Medica Iranica
|July 21, 2017
PubMed

Insights

The methionine synthase (MTR) A2756G gene variant is linked to an increased risk of prostate cancer in men. This genetic variation may alter enzyme function, potentially serving as a biomarker for cancer susceptibility.

Area of Science:

  • Genetics
  • Molecular Biology
  • Oncology

Background:

  • The methionine synthase (MTR) enzyme is crucial for DNA methylation and repair via the folate pathway.
  • Prostate cancer is a significant health concern, and understanding its genetic risk factors is vital.

Purpose of the Study:

  • To investigate the association between the MTR A2756G gene polymorphism and prostate cancer risk in a Kashan-Iran male population.
  • To evaluate the in silico effects of the A2756G transition on MTR enzyme structure and function.

Main Methods:

  • A case-control study involving 100 prostate cancer patients and 100 healthy controls.
  • Genotyping of the MTR A2756G polymorphism using the PCR-RFLP technique.
  • In silico analysis to predict the impact of the polymorphism on MTR protein properties.

Main Results:

  • The AG genotype (OR: 2.40, P=0.004) and GG genotype (OR: 3.63, P=0.017) of MTR A2756G were significantly associated with increased prostate cancer risk.
  • The G allele also showed a significant association with prostate cancer (OR: 2.01, P=0.0014).
  • In silico analysis suggested that the A2756G polymorphism may alter MTR enzyme stability and function.

Conclusions:

  • The MTR A2756G polymorphism is associated with prostate cancer susceptibility in the studied male population.
  • This genetic variation may influence enzyme activity and stability, contributing to cancer risk.
  • Further comprehensive studies are warranted to establish this polymorphism as a clinical biomarker for prostate cancer.