Advanced Biomedical Research (Jan 2023)

Evaluation of Rap1GAP and EPAC1 gene expression in endometriosis disease

  • Mehran Dehghanian,
  • Ghafour Yarahmadi,
  • Reyhaneh Sadat Sandoghsaz,
  • Ali Khodadadian,
  • Farimah Shamsi,
  • Mohammad Yahya Vahidi Mehrjardi

DOI
https://doi.org/10.4103/abr.abr_86_22
Journal volume & issue
Vol. 12, no. 1
pp. 101 – 101

Abstract

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Background: Endometriosis is a female reproductive system disease in which the endometrial tissue is found in other women's organs. Various factors are effective in the development of endometriosis, and because of the interaction of genetics and environmental factors, this disease is a multi-factorial disease. MAPK/ERK and PI3K/Akt/mTOR pathways are activated by growth factors and steroid hormones and are known as two important pathways involved in the processes of growth, proliferation, and survival of endometriosis cells. Raps, monomeric GTPase of the Ras family, are able to activate these pathways independent of Ras. The goal of our study was to evaluate the expression level of Rap1GAP and EPAC1 genes as two important RapGAPs (GTPase-activating proteins) and RapGEFs (guanine nucleotide exchange factors), respectively, in endometriosis tissues and normal endometrium tissues. Materials and Methods: In this study, 15 samples of women without signs of endometriosis were taken as control samples. Fifteen ectopic and 15 eutopic samples were taken from women with endometriosis using laparoscopic surgery. The expression of EPAC1 and Rap1GAP genes was investigated by the real-time polymerase chain reaction technique, and the results were analyzed by one-way ANOVA test. Results: EPAC1 upregulated significantly in ectopic tissues compared to eutopic and control tissues. Rap1GAP expression was lower in ectopic tissues compared to control and eutopic tissues. Conclusions: Based on these results, it may be concluded that changes in the expression of the Rap1GAP and Epca1 genes may play a role in the pathways involved in the pathogenesis, displacement, and migration of endometriosis cells.

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