Evaluation of Rap1GAP and Epac1 Gene Expression in Endometriosis

Abstract

Objective: Endometriosis is a female reproductive system disease in which endometrial tissue are found in other women organs. Various factors are effective in the development of endometriosis and due to the interaction of genetics and environmental factors, this disease is a multifactorial disease. MAPK/ERK and PI3K/Akt/mTOR pathways are activated by growth factors and steroid hormones and known as two important pathways involved in the processes of growth, proliferation and survival of endometriosis cells. Raps, monomeric GTPase of Ras family, are able to activate these pathways independently of Ras. The goal of our study was to evaluated the expression level of Rap1GAP and Epac1 gene, 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, 15 ectopic and 15 eutopic samples were taken from women with endometriosis using laparoscopic surgery. The expression of Epac1 and Rap1GAP genes was investigated by Real-time PCR technique and results were analysis by One-Way ANOVA test.Results: Epac1 upregulated significantly in ectopic tissues compared to eutopic and control tissues (Their P-value were <0.0001). Rap1GAP expression was lower in ectopic tissues compared to control samples (P-value was 0.003) and eutopic tissues (P-value was 0.001).Conclusion: Based on these results, it may be concluded that changes in the expression of the Rap1GAP and Epca1 genes may play role in the pathways involved in the pathogenesis, displacement, and migration of endometriosis cells.

Screening and identification of key biomarkers associated with endometriosis using bioinformatics and next generation sequencing data analysis

“…Signaling pathways include extracellular matrix organization [101], nervous system development [102], signal transduction [103], hemostasis [104], muscle contraction [105], signaling by retinoic acid [106] and diseases of glycosylation [107] were responsible for advancement of endometriosis. Altered expression of L1CAM [108], HSD17B2 [109], VCAM1 [110], SOX6 [111], FGF10 [112], MMP12 [113], CCR1 [114], PROK1 [115], PRL (prolactin) [116], TIMP3 [117], ADAMTS9 [118], NDNF (neuron derived neurotrophic factor) [119], LHCGR (luteinizing hormone/choriogonadotropin receptor) [120], PDGFB (platelet derived growth factor subunit B) [121], LDLR (low density lipoprotein receptor) [122], CD4 [123], FOXL2 [124], TRPA1 [125], ADRB2 [126], PLAU (plasminogen activator, urokinase) [127], EPCAM (epithelial cell adhesion molecule) [128], UCN2 [129], CYP1A1 [130], NTN1 [131], IL15 [132], BMP2 [133], APOE (apolipoprotein E) [134], CASP1 [135], ABCG2 [136], ACE (angiotensin I converting enzyme) [137], PGR (progesterone receptor) [138], ALPP (alkaline phosphatase, placental) [139], LPAR4 [140], ATRNL1 [141], HLA-C [142], MMP3 [143], PDLIM3 [144], NFASC (neurofascin) [145], IL33 [146], NGF (nerve growth factor) [147], COMP (cartilage oligomeric matrix protein) [148], FST (follistatin) [149], EFEMP1 [150], GATA6 [151], TCF21 [152], PTGS2 [153], HOXC8 [154], AKR1C3 [155], BDNF (brain derived neurotrophic factor) [119], EPHA3 [156], INHBA (inhibin subunit beta A) [157], RAP1GAP [158], TLR3 [159], NOX4 [160], TGFBI (transforming growth factor beta induced) [161], IGF2BP1 [162], DLX5 [163], VDR (vitamin D receptor) [164], F...…”

Cordycepin Triphosphate as a Potential Modulator of Cellular Plasticity in Cancer via cAMP-Dependent Pathways: An In Silico Approach

“…The following supporting information can be downloaded at . References [ 105 , 145 , 146 , 147 , 148 , 149 , 150 , 151 , 152 , 153 , 154 , 155 , 156 , 157 , 158 , 159 , 160 , 161 , 162 , 163 , 164 , 165 , 166 ] are cited in the Supplementary Material.…”