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Construction of Circrna-Mirna-Mrna Network in the Pathogenesis of Recurrent Implantation Failure Using Integrated Bioinformatics Study Publisher Pubmed



Ahmadi M1, 2, 3 ; Pashangzadeh S4 ; Moraghebi M1 ; Sabetian S5 ; Shekari M2 ; Eini F6 ; Salehi E6 ; Mousavi P2, 6
Authors
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Authors Affiliations
  1. 1. Student Research Committee, Hormozgan University of Medical Sciences, Bandar Abbas, Iran
  2. 2. Department of Medical Genetics, Faculty of Medicine, Hormozgan University of Medical Sciences, Bandar Abbas, Iran
  3. 3. Division of Medical Genetics, Booali Medical Diagnostic Laboratory, Qom, Iran
  4. 4. Iranian Research Center for HIV/AIDS, Iranian Institute for Reduction of High-Risk Behaviors, Tehran University of Medical Sciences, Tehran, Iran
  5. 5. Infertility Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
  6. 6. Fertility and Infertility Research Center, Hormozgan University of Medical Sciences, Bandar Abbas, Iran

Source: Journal of Cellular and Molecular Medicine Published:2022


Abstract

This research attempted to elucidate the molecular components are involved in the pathogenesis of recurrent implantation failure (RIF). We initially identified that 386 mRNAs, 144 miRNAs and 2548 circRNAs were differentially expressed (DE) in RIF and then investigated the genetic cause of the observed abnormal expression by constructing a circRNA-miRNA-mRNA network considering the competing endogenous RNA theory. We further analysed the upstream transcription factors and related kinases of DEmRNAs (DEMs) and demonstrated that SUZ12, AR, TP63, NANOG, and TCF3 were the top five TFs binding to these DEMs. Besides, protein-protein interaction analysis disclosed that ACTB, CXCL10, PTGS2, CXCL12, GNG4, AGT, CXCL11, SST, PENK, and FOXM1 were the top 10 hub genes in the acquired network. Finally, we performed the functional enrichment analysis and found that arrhythmogenic right ventricular cardiomyopathy (ARVC), hypertrophic cardiomyopathy (HCM), pathways in cancer, TNF signalling pathway and steroid hormone biosynthesis were the potentially disrupted pathways in RIF patients. Optimistically, our findings may deepen our apprehensions about the underlying molecular and biological causes of RIF and provide vital clues for future laboratory and clinical experiments that will ultimately bring a better outcome for patients with RIF. © 2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.
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